1. RENAL 2. LIVER 3.PANCREAS 4. SPLEEN 5. SKIN 6. VESSELS WALLS

PIGMENT & TISSUE DEPOSITS Flashcards by Christine Joyce

types of lipids which can accumulate:

TRIGLYCERIDES
INHERITED STORAGE DISEASE
CHOLESTEROL ACCUMULATION

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2 Types of lipid accumulation:

INTRACELLULAR
ADIPOSE TISSUE INFILTRATION

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adipos tissue infiltration can be seen in?

SKELETAL AND MYOCARDIAL

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adipose tissue infiltration sometimes called?

muscle steatosis

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

ATHEROSCLEROSIS

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

XANTHOMAS

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excessive intracellular deposits of glycogen, seen in glycogen metabolis.

GLUCOSE ACCUMULATION

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3 types of accumulation:

LIPID ACCUMULATION
GLYCOGEN ACCUMULATION
PROTEIN ACCUMULATION

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

HYALINE

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

FIBRINOID

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

FIBRINOID NECROSIS

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

RUSSEL BODIES OF PLASMA CELLS

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defects in protein folding can cause:

“unfolded protein response”-
aggregates of misfolded proteins

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

AMYLOID

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

AMYLOID FIBRILS

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

AMYLOIDOSIS

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Most common form of amyloid:

PROTEIN AA
PROTEIN AL
FAMILIAL AMYLOID
ENDOCRINE AMYLOID
OTHER AMYLOID

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

PROTEIN AA

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derived from immunoglobulin light chain w/ plasma cell.

PROTEIN AL

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eg. sharpei dogs, abyssian cat

FAMILIAL AMYLOID

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

ENDOCRINE AMYLOID

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example are misfolded protein and amyloid plaques

OTHER AMYLOIDES

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gross appearnce of amyloid:

ORGAN- normal/enlarged
2.STAIN- BROWN OR BLACK

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site of amyloid:

RENAL
LIVER
3.PANCREAS
SPLEEN
SKIN
VESSELS WALLS

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Types of endogenous pigments:

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

also known as "wear & tear" & " aging pigment"

lipofuscin

site of lipofuscin :

1. AGED CELLS 2. MYOCARDIAL CELLS 3. NEURONS 4. CHRONICALLY INIJURED CELLS

gross apearance of lipofuscin:

YELLOW - BROWN discoloration of tissue

microscope appearance:

1.GOLDEN BROWN 2. GRANULAR 3. INTRACELLULAR PIGMENT

significance of lipofuscin:

does not injured cell/ but shows sign of aging

disorders characterized by the excess storage of lipofuscin.

LIPOFUSCINOSIS

variant of lipofuscin which is acid-fast positive and autofluorescent

CEROID

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

MELANIN

Location of melanin:

SKIN, HAIR, EYES,

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

MELANOSIS

gross appearance of melanosis:

1. DARK PIGMENT

microscope appearance of melanosis:

1. FINELY GRANULAR 2. BROWN INTRACELLULAR

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.

COPPER

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

COPPER TOXICITY

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

SHEEP

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

HEMOSIDERIN

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

HEMOSIDERIN GRANULES

Sites of hemosiderin:

1. SPLEEN 2. BONE MARROW

Gross appearance of hemosiderin:

LIGHT BROWN COLOR

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

HEMATOCHROMATOSIS

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

BILIRUBIN

3 occurence of bilirubin:

1. PRE- HEPATIC JAUNDICE 2. HEPATIC JAUNDICE 3. POST HEPATIC JAUNDICE

failure of conjugation or excretions.

HEPATIC JAUNDICE

obstruction of bile duct

POST HEPATIC JAUNDICE

increased breakdown of erythrocytes

PRE-HEPATIC JAUNDICE

Gross appearance of bilirubin:

blood and tissue produce YELLOW DISCOLORATION called "JAUNDICE OR ICTERUS"

Microscope appearance of bilirubin:

GREEN- BROWN TO YELLOW - BROWN GRANULAR PIGMENT

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

HEMATOIDIN

blood + acid = acid hematin (black color)

ACID- HEMATIN

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

MELENA

refers to the deposition of calcium salts in soft tissues.

PATHOLOGIC CALCIFICATION

2 TYPES OF CALCIFICATION

1. DYSTROPHIC CALCIFICATION 2. METASTIC CALCIFICATION

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

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

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

METASTIC CALCIFICATION

Term sometimes used for extensive metastatic calcification is

CALCINOSIS

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

CALCIPHYLAXIS

EXAMPLE OF CRYSTALS :

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

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

GOUT

uric acid is the end product of

NITROGEN METABOLISM

Gross appearance of gout:

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

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

CHOLESTEROL CLEFTS

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

EXOGENOUS PIGMENTS

are those that originate in the animal.

ENDOGENOUS PIGMENTS

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

ANTHRACOSIS

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

SILICOSIS

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

ABESTOSIS

Pnuemonyssus simicola Plasmodia Fasciolodes magna are example of:?

PARASITIC PIGMENT

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

PNEUMONYSSUS SIMICOLA

malarial pigment from excretion of catabolized hemoglobin

PLASMODIA

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

FASCIOLODES MAGNA

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

SERUM

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

ALANINE TRANSAMINASE

-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.

ASPARTATE TRANSAMINASE

OTHER ENZYME USED TO EVALUATE TISSUE DAMAGE:

1. ACETIC DEHYDROGENASE 2. CREATINE PHOSPHOKINASE 3. ALKALINE PHOSPHATE