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Form & Function 1 > Lecture 58 - Gen Path Pigments > Flashcards

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

A

Liver

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

A

heart

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
Q

write the steps of erythrocyte breakdown

A
  1. heme
  2. biliverdin
  3. bilirubin
  4. conjugation in liver
  5. urobilinogen in GIT
26
Q

what causes icterus

A

hyperbilirubinemia

27
Q

what are the causes of hyperbilirubinemia

A
  1. pre-hepatic (hemolysis)
  2. hepatic (liver disease; unconjugated form)
  3. post-hepatic (obstruction of bile flow; conjugated form)
28
Q

what is the only endogenous black-brown pigment

A

melanin

29
Q

what locations are melanin pathologic

A

melanocytic neoplasms
hyperpigmentation in skin

30
Q

what causes black pigment in tissues

A

pesudomelanosis (hydrogen sulfide producing bacteria)

anthracosis (carbon dust accumulation)

31
Q

amyloidosis

A
  • protein-folding disorder resulting in insoluble amyloid
  • predominantly extracellular
  • local or systemic
32
Q

what forms of amyloid are there

A
  1. AA (amyloid A)
  2. AL (amyloid light chain)
  3. IAPP (Islet associated polypeptide)
  4. AB (amyloid beta)
33
Q

describe AA

A
  • serum amyloid A (positive acute phase protein)
  • hereditary to share pei, Abyssinian, and Siamese
34
Q

describe AL

A
  • derived from light chains of antibodies
  • B-cell neoplasms or blood disorders
35
Q

Describe IAPP

A
  • associated with diabetes in humans
36
Q

describe AB

A
  • found in neural plaques of Alzheimer’s
37
Q

describe the gross anatomy of amyloid

A

enlarged, waxy, pale organs
dark brown with iodine

38
Q

describe the histomorphology of amyloid

A

pink color

present at space of disse in liver = pressure atrophy of hepatic cords

lymphoid follicles in spleen

glomeruli of kidneys = protein loss

39
Q

what are the two kinds of mineralization?

A
  1. dystrophic calcification
  2. metastatic calcification
40
Q

describe dystrophic calcification

A

within mitochondria or membrane-bound matrix vesicles

gross: fine, white granules or clumps
histology: basophilic, granular

41
Q

describe metastatic mineralization

A

systemic Ca:P imbalance where the product is elevated (intercostal pleura, kidney, stomach, lungs, etc.)

42
Q

what are the causes of metastatic mineralization

A

renal disease (↑ P)
hypervitaminosis D
bone turnover (↑ Ca)
hyperparathyroidism
PTH related protein (↑ Ca)

43
Q

T/F: a functional tumor produces a hormone

A

TRUE

44
Q

T/F: primary hyperparathyroidism is concurrent with renal disease

A

FALSE - secondary

Form & Function 1 (66 decks)

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