PIGMENT & TISSUE DEPOSITS Flashcards
types of lipids which can accumulate:
- TRIGLYCERIDES
- INHERITED STORAGE DISEASE
- CHOLESTEROL ACCUMULATION
2 Types of lipid accumulation:
- INTRACELLULAR
- ADIPOSE TISSUE INFILTRATION
adipos tissue infiltration can be seen in?
SKELETAL AND MYOCARDIAL
adipose tissue infiltration sometimes called?
muscle steatosis
accumulation of lipids in smooth muscle cells
and macrophages in walls of arteries / arterioles
ATHEROSCLEROSIS
tumor like masses in skin formed by clusters of
foamy macrophages; seen with inherited or acquired hyperlipidemic states.
XANTHOMAS
excessive intracellular deposits of glycogen, seen in glycogen metabolis.
GLUCOSE ACCUMULATION
3 types of accumulation:
- LIPID ACCUMULATION
- GLYCOGEN ACCUMULATION
- PROTEIN ACCUMULATION
is the name given to any substance, intracellular or extracellular, which has a homogeneous, glassy, eosinophilic appearance;
This is “protein in nature”
HYALINE
is a nonspecific term for hyaline material within an arterial wall.
FIBRINOID
the presence of plasma proteins / Ag-Ab / complement within a damaged vascular wall causes intense eosinophilic staining
FIBRINOID NECROSIS
a result of immunoglobulin
accumulating in the cisternae of the RER.
RUSSEL BODIES OF PLASMA CELLS
defects in protein folding can cause:
- “unfolded protein response”-
- aggregates of misfolded proteins
a pathologic proteinaceous substance
(95% amyloid fibrils) which is resistant to proteolysis.
AMYLOID
are insoluble aggregates that result from the self-assembly of abnormally folded proteins
AMYLOID FIBRILS
a disorder of protein folding in which normally soluble proteins are deposited as abnormal, insoluble fibrils that disrupt tissue structure and
function.
AMYLOIDOSIS
Most common form of amyloid:
- PROTEIN AA
- PROTEIN AL
- FAMILIAL AMYLOID
- ENDOCRINE AMYLOID
- OTHER AMYLOID
an “acute-phase” protein calles SERUM AMYLOID A in chronic inflammation.
PROTEIN AA
derived from immunoglobulin light chain w/ plasma cell.
PROTEIN AL
eg. sharpei dogs, abyssian cat
FAMILIAL AMYLOID
this is derived from polypeptide hormones or phoromones in neoplastic or denegerative
ENDOCRINE AMYLOID
example are misfolded protein and amyloid plaques
OTHER AMYLOIDES
gross appearnce of amyloid:
- ORGAN- normal/enlarged
2.STAIN- BROWN OR BLACK
site of amyloid:
- RENAL
- LIVER
3.PANCREAS - SPLEEN
- SKIN
- VESSELS WALLS
Types of endogenous pigments:
- LIPOFUSCIN
- CEROID
- MELANIN
- COPPER
- HEMOSIDERIN
- BILIRUBIN
- HEMATOIDIN
- ACID-HEMATIN
also known as “wear & tear” & “ aging pigment”
lipofuscin
site of lipofuscin :
- AGED CELLS
- MYOCARDIAL CELLS
- NEURONS
- 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:
- DARK PIGMENT
microscope appearance of melanosis:
- FINELY GRANULAR
- 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:
- SPLEEN
- 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:
- PRE- HEPATIC JAUNDICE
- HEPATIC JAUNDICE
- 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
- DYSTROPHIC CALCIFICATION
- 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 :
- CALCIUM OXALATE
- URATES & URIC ACID
- 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:
- ACETIC DEHYDROGENASE
- CREATINE PHOSPHOKINASE
- ALKALINE PHOSPHATE
