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PATHOLOGY > PIGMENT & TISSUE DEPOSITS > Flashcards

PIGMENT & TISSUE DEPOSITS Flashcards

1
Q

types of lipids which can accumulate:

A
  1. TRIGLYCERIDES
  2. INHERITED STORAGE DISEASE
  3. CHOLESTEROL ACCUMULATION
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2
Q

2 Types of lipid accumulation:

A
  1. INTRACELLULAR
  2. ADIPOSE TISSUE INFILTRATION
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3
Q

adipos tissue infiltration can be seen in?

A

SKELETAL AND MYOCARDIAL

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4
Q

adipose tissue infiltration sometimes called?

A

muscle steatosis

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5
Q

accumulation of lipids in smooth muscle cells
and macrophages in walls of arteries / arterioles

A

ATHEROSCLEROSIS

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6
Q

tumor like masses in skin formed by clusters of
foamy macrophages; seen with inherited or acquired hyperlipidemic states.

A

XANTHOMAS

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7
Q

excessive intracellular deposits of glycogen, seen in glycogen metabolis.

A

GLUCOSE ACCUMULATION

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8
Q

3 types of accumulation:

A
  1. LIPID ACCUMULATION
  2. GLYCOGEN ACCUMULATION
  3. PROTEIN ACCUMULATION
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9
Q

is the name given to any substance, intracellular or extracellular, which has a homogeneous, glassy, eosinophilic appearance;
This is “protein in nature”

A

HYALINE

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10
Q

is a nonspecific term for hyaline material within an arterial wall.

A

FIBRINOID

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11
Q

the presence of plasma proteins / Ag-Ab / complement within a damaged vascular wall causes intense eosinophilic staining

A

FIBRINOID NECROSIS

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12
Q

a result of immunoglobulin
accumulating in the cisternae of the RER.

A

RUSSEL BODIES OF PLASMA CELLS

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13
Q

defects in protein folding can cause:

A
  1. “unfolded protein response”-
  2. aggregates of misfolded proteins
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14
Q

a pathologic proteinaceous substance
(95% amyloid fibrils) which is resistant to proteolysis.

A

AMYLOID

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15
Q

are insoluble aggregates that result from the self-assembly of abnormally folded proteins

A

AMYLOID FIBRILS

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16
Q

a disorder of protein folding in which normally soluble proteins are deposited as abnormal, insoluble fibrils that disrupt tissue structure and
function.

A

AMYLOIDOSIS

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17
Q

Most common form of amyloid:

A
  1. PROTEIN AA
  2. PROTEIN AL
  3. FAMILIAL AMYLOID
  4. ENDOCRINE AMYLOID
  5. OTHER AMYLOID
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18
Q

an “acute-phase” protein calles SERUM AMYLOID A in chronic inflammation.

A

PROTEIN AA

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19
Q

derived from immunoglobulin light chain w/ plasma cell.

A

PROTEIN AL

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20
Q

eg. sharpei dogs, abyssian cat

A

FAMILIAL AMYLOID

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21
Q

this is derived from polypeptide hormones or phoromones in neoplastic or denegerative

A

ENDOCRINE AMYLOID

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22
Q

example are misfolded protein and amyloid plaques

A

OTHER AMYLOIDES

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23
Q

gross appearnce of amyloid:

A
  1. ORGAN- normal/enlarged
    2.STAIN- BROWN OR BLACK
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24
Q

site of amyloid:

A
  1. RENAL
  2. LIVER
    3.PANCREAS
  3. SPLEEN
  4. SKIN
  5. VESSELS WALLS
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25
Q

Types of endogenous pigments:

A
  1. LIPOFUSCIN
  2. CEROID
  3. MELANIN
  4. COPPER
  5. HEMOSIDERIN
  6. BILIRUBIN
  7. HEMATOIDIN
  8. ACID-HEMATIN
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26
Q

also known as “wear & tear” & “ aging pigment”

A

lipofuscin

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27
Q

site of lipofuscin :

A
  1. AGED CELLS
  2. MYOCARDIAL CELLS
  3. NEURONS
  4. CHRONICALLY INIJURED CELLS
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28
Q

gross apearance of lipofuscin:

A

YELLOW - BROWN discoloration of tissue

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29
Q

microscope appearance:

A

1.GOLDEN BROWN
2. GRANULAR
3. INTRACELLULAR PIGMENT

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30
Q

significance of lipofuscin:

A

does not injured cell/ but shows sign of aging

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31
Q

disorders characterized by the excess storage of lipofuscin.

A

LIPOFUSCINOSIS

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32
Q

variant of lipofuscin which is acid-fast positive and autofluorescent

A

CEROID

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33
Q

insoluble, intracellular, brown-black pigment derived from tyrosine.

A

MELANIN

34
Q

Location of melanin:

A

SKIN, HAIR, EYES,

35
Q

melanin can also occur incidentally at other sites and when in excess CALLED?

A

MELANOSIS

36
Q

gross appearance of melanosis:

A
  1. DARK PIGMENT
37
Q

microscope appearance of melanosis:

A
  1. FINELY GRANULAR
  2. BROWN INTRACELLULAR
38
Q

an essential trace element; the liver is the major organ involved in the
regulation of copper levels, and homeostasis is maintained by the
balance of dietary intake and copper excretion via the bile.

A

COPPER

39
Q

storage of large amounts of copper is toxic to the hepatocyte and may produce a sudden onset of acute hepatocellular
degeneration

A

COPPER TOXICITY

40
Q

copper toxicity is common in this animals, because of the reduced billaru secretion

A

SHEEP

41
Q

represents stored iron (ferric form = Fe3+), recovered from the hemoglobin of destroyed rbc’s.

A

HEMOSIDERIN

42
Q

Fe3 bound to apoferritin forming derritin excess ferritin forms what??

A

HEMOSIDERIN GRANULES

43
Q

Sites of hemosiderin:

A
  1. SPLEEN
  2. BONE MARROW
44
Q

Gross appearance of hemosiderin:

A

LIGHT BROWN COLOR

45
Q

when a massive accumulation of iron
causes cell damage; common in humans, rare in other species

A

HEMATOCHROMATOSIS

46
Q

bilirubin is end product of heme degradation (no iron); mostly from senescent rbc’s via macrophages.

A

BILIRUBIN

47
Q

3 occurence of bilirubin:

A
  1. PRE- HEPATIC JAUNDICE
  2. HEPATIC JAUNDICE
  3. POST HEPATIC JAUNDICE
48
Q

failure of conjugation or excretions.

A

HEPATIC JAUNDICE

49
Q

obstruction of bile duct

A

POST HEPATIC JAUNDICE

50
Q

increased breakdown of erythrocytes

A

PRE-HEPATIC JAUNDICE

51
Q

Gross appearance of bilirubin:

A

blood and tissue produce YELLOW DISCOLORATION called “JAUNDICE OR ICTERUS”

52
Q

Microscope appearance of bilirubin:

A

GREEN- BROWN TO YELLOW - BROWN GRANULAR PIGMENT

53
Q

bright yellow-brown homogenous pigment occasionally seen at sites
of previous hemorrhage. believed to be locally precipitated bilirubin (stains negative for iron).

A

HEMATOIDIN

54
Q

blood + acid = acid hematin (black color)

A

ACID- HEMATIN

55
Q

imparts black color to blood originating in stomach (eg gastric ulcers),
ie blood + stomach HCl =

A

MELENA

56
Q

refers to the deposition of calcium salts in soft tissues.

A

PATHOLOGIC CALCIFICATION

57
Q

2 TYPES OF CALCIFICATION

A
  1. DYSTROPHIC CALCIFICATION
  2. METASTIC CALCIFICATION
58
Q

eg,“white muscle disease”
gross appearance is:
stain in VON KOSSA
and is not associated w/ hypercalcemia

A

-DYSTROPHIC CALCIFICATION
1. WHITE/DRY /GRITTY
2. BLACK

59
Q

Deposition of calcium salts in vital tissues and is always associated with
hypercalcemia

A

METASTIC CALCIFICATION

60
Q

Term sometimes used for extensive metastatic calcification is

A

CALCINOSIS

61
Q

is a term that describes widespread of deposition of
calcium in tissues of individual treated with a calcium sensitizer.

A

CALCIPHYLAXIS

62
Q

EXAMPLE OF CRYSTALS :

A
  1. CALCIUM OXALATE
  2. URATES & URIC ACID
  3. CHOLESTEROL CLEFTS
63
Q

disorder of purine metabolism with hyperuricemia and deposition of urates in tissues.

A

GOUT

64
Q

uric acid is the end product of

A

NITROGEN METABOLISM

65
Q

Gross appearance of gout:

A

chalky white masses in tissues (called “tophi”) or “frosting” of crystals on serosal membranes.

66
Q

elongate, needle-like crystals, often in picket fence- type arrangement.

A

CHOLESTEROL CLEFTS

67
Q

are those that originate outside the body, ie from external environment.

A

EXOGENOUS PIGMENTS

68
Q

are those that originate in the
animal.

A

ENDOGENOUS PIGMENTS

69
Q

deposition of carbon particles, gives tissue a black discoloration to tissue, relatively harmless unless present in large quantities, draining lymph nodes.

A

ANTHRACOSIS

70
Q

deposition of silica dust in the lungs, is a special problem for miners;
causes granulomatous pneumonia.

A

SILICOSIS

71
Q

deposition of asbestos into lung, associated with mesotheliomas, and
chronic lung injury.

A

ABESTOSIS

72
Q

Pnuemonyssus simicola
Plasmodia
Fasciolodes magna
are example of:?

A

PARASITIC PIGMENT

73
Q

brown to black pigment in the airways of
monkeys with lung mites.

A

PNEUMONYSSUS SIMICOLA

74
Q

malarial pigment from excretion of catabolized hemoglobin

A

PLASMODIA

75
Q

liver fluke of ruminants; see black discoloration of tissue around bile ducts due to regurgitated iron-porphyrin pigment
(“fluke puke”).

A

FASCIOLODES MAGNA

76
Q

Degenerating and necrotizing cells leak enzymes from cytoplasm into the blood
and can be measured in?

A

SERUM

77
Q
  • called as serum glutamic pyruvic
    transaminase (SGPT)
  • is released from the cytoplasm of injured liver
    cells. (in moderate injury).
A

ALANINE TRANSAMINASE

78
Q

-called serum glutamic-oxaloacetic
transaminase (SGOT),
-located in mitochondria and is released in more extensive injury.
-occurs in liver, muscles etc.
But take note that it is not tissue specific as in ALT.

A

ASPARTATE TRANSAMINASE

79
Q

OTHER ENZYME USED TO EVALUATE TISSUE DAMAGE:

A
  1. ACETIC DEHYDROGENASE
  2. CREATINE PHOSPHOKINASE
  3. ALKALINE PHOSPHATE
80
Q
A

PATHOLOGY (23 decks)

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