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144 Cards in this Set

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3 categories of intracellular accumulations
1. A normal cellular constituent accumulated in excess – H2O, lipids, proteins, CHO
2. An abnormal substance – endogenous or exogenous
3. Pigments - endogenous or exogenous
3 mechanisms or types of processes of I/C accumulations
1. Incr rate of production and/or decr rate of removal – fatty change in the liver, protein droplets in renal prox tubular cells due to increased leakage from glomeruli
2. Defects in the metabolism, packaging, transport or secretion – lysosomal storage diseases
3. Inability to degrade the exogenous substances – carbon, silica
prototype of accumulation of lipids
hepatic lipidosis
5 mechanisms of hepatic lipidosis or steatosis
1. Excessive delivery of FFAs either from the gut or from adipose tissue
2. Decreased β-oxidation of FAs to ketones and other substances b/c of mitochondrial injury (toxins, hypoxia)
3. Impaired synthesis of apoprotein (CCl4, aflatoxin)
4. Impaired combination of TGs and protein to form lipoprotein (uncommon)
5. Impaired release of LPs from the hepatocyte (uncommon)
another term for lipidosis
If severe - enlarged, yellow, soft and friable; rounded edges of lobes; Cut surface – bulge, soft, friable, of greasy texture; If severe, sections float in formalin; Important to distinguish from glucocorticoid hepatopathy (accumulation of glycogen) in dogs
gross examination of fatty liver in hepatic lipidosis
Initially a few small clear vacuoles → eventually coalesce into larger vacuoles; Vacuoles sharply delineated; Nucleus may be displaced; Need to be distinguished from glycogen and water (hydropic degeneration); Special stains – Oil-red-O for fat; PAS for glycogen; water not stained
microscopic examination of hepatic lipidosis with varying degrees of cytoplasmic vacuolation
3 causes of accumulation of glycogen
1. DM
2. excess corticosteroids Rx (most common)
3. glycogen storage disease (glycogenesis)
5 causes of accumulation of proteins
1. Reabsorption droplets in proximal renal tubular cells – in proteinuria
2. Excessive production of normal proteins – Russell bodies (Mott cells-type of plasma cells which are full of Ab’s)
3. Defective I/C transport and secretion of critical proteins
4. Accumulation of cytoskeletal proteins (Alcoholic hyaline – an eosinophilic cytoplasmic inclusion in liver cells composed of keratin IF)
5. Aggregation of abnormal proteins – I/C or E/C deposits of abnormal or misfolded proteins (proteinopathies)
an eosinophilic cytoplasmic inclusion in liver cells composed of keratin IF
alcoholic hyaline
– a descriptive term that refers to an alteration within cells or in the E/C space that gives a homogeneous, glassy, pink appearance in routine histologic sections
examples include Reabsorption droplets, Russell bodies, alcoholic hyaline
I/C hyaline
example of ____ _____ is hyalinized walls of arterioles in the kidney in longstanding hypertension and diabetes mellitus
E/C hyaline
examples include Autophagic vacuoles; Crystalline protein inclusion bodies (Crystalloids) – in hepatocytes and renal tubular cells in old dogs, unknown significance;
Viral inclusion bodies; Lead inclusion bodies
other I/C inclusions
type of plasma cells which are full of Ab’s
mott cells
examples of _____ _____ include Hyaline casts in the lumens of renal tubules (proteinuria), Serum or plasma in blood vessels, Plasma proteins in vessel walls (ex. porcine edema disease), Old scars (collagen), Thickened BM (glomerulonephritis), Hyaline membranes of the alveolar walls (leakage of alveolar capillaries), Hyaline microthrombi (DIC), Amyloid
hyaline substances
hyaline substances are examples of ______ ______
extracellular accumulations
a pathologic proteinaceous substance deposited in the extracellular space in various tissues and organs of the body
what is the physical nature of amyloid
beta-pleated sheet conformation
what is the chemical nature of amyloid
95% fibril proteins, 5% P component and other glycoproteins
how many biochemically distinct forms of amyloid proteins
what are the 3 most common forms of amyloid proteins
AL, AA, AB (beta)
derived from Ig light chains produced in plasma cells
AL (amyloid light chain)
derived from a unique non-Ig protein synthesized by the liver
AA (amyloid-associated)
precursor of AA fibrils and found in the serum
SAA (serum amyloid-associated)
The production of ___ protein is increased in inflammatory states as part of the “acute phase response”, therefore, is associated with chronic inflammation, and is often called ______ ______.
SAA; secondary amyloidosis
produced from a precursor protein and is found in the cerebral lesions of Alzheimer disease
AB (beta) amyloid
3 other proteins found in amyloid depostis
transthyretin (TTR), B2-microglobulin, prion proteins
a normal serum protein that binds and transports thyroxine and retinol; A mutant form of this is deposited in a group of familial amyloid polyneuropathies.
transthyretin (TTR)
a component of MHC-I molecules and a normal serum protein, has been identified as the amyloid fibril subunit (Aβ2m) in amyloidosis associated with long-term hemodialysis.
in a minority of cases of ____ disease, the misfolded _____ proteins aggregate in the extracellular space w/n the CNS and acquire the structural and staining characteristics of amyloid protein
prion (prion proteins)
3 other minor components in amyloid
serum amyloid P component, proteoglycans, and highly sulfated GAGs.
serum amyloid P component, proteoglycans, and highly sulfated GAGs.
When the cut surface of an affected kidney is treated with iodine solution, then w/ dilute sulfuric acid, it turns blue – hence the name meaning “starch-like”
____-____ stains amyloid orange to orange red and imparts apple green fluorescence on histologic sections
Common tissues affected in animals – kidney, spleen, LN, liver, islets (cats), endocrine tumors, GI; Systemic
by amyloid
an abnormal condition of the blood or bone marrow.
the most common form of amyloidosis in human, not in animals
plasma cell dyscrasia
common form of amyloidosis in animals
Reactive systemic amyloidosis (secondary amyloidosis)
4 other E/C accumulations besides amyloidosis
fibrinoid change, gout, psuedogout, cholesterol crystals
a hyaline deposition of Ig, C, &/or plasma proteins including fibrin in the vascular wall, due to injury to the intima and media such as in IM vasculitides
fibrinoid change
deposition of Na urate crystals or urates in tissue in humans, birds and reptiles
deposition of Ca pyrophosphate crystals in humans, nonhuman primates
by-products of hemorrhage and necrosis; E/C accumulation
cholesterol crystals
Abnormal tissue deposition of Ca phosphates or carbonates in dead or normal tissues, together with smaller amount of Fe, Mg and other mineral salts
pathologic calcification
deposition of Ca in dying tissues despite normal serum levels of Ca and in the absence of derangements in Ca metabolism
dystrophic calcification
deposition of Ca salts in otherwise normal tissues - results from hypercalcemia
metastatic calcification
deposition of Ca salts in otherwise normal tissues - results from hypercalcemia
calcification morphology
Microscopic - Basophilic, granular, sometimes clumped appearance
calcification morphology
Almost always results from hypercalcemia; Common location of Ca deposition - Gastric mucosa, kidneys, lungs, systemic arteries, and pulmonary veins
metastatic calcification
4 causes of hypercalcemia
Renal failure;Vitamin D toxicosis; PTH and PTH-related protein (Primary hyperparathyroidism - rare; Hypercalcemia associated w/ canine lymphomas and apocrine carcinomas of the anal sac); Destruction of bone from primary or metastatic tumors
Production of bone at an abnormal site
heterotopic (ectopic) bone
foci of cells or tissues, which are microscopically normal but present at an abnormal location
2 types of ectopic bone
heterotopic; osseous metaplasia
Substances that are inherently colored
________ is most common pigment along with ______ (________ is not important in pathology except in a few exceptions)
hemoglobin; melanin; melanin
what is the most abundant mesenchymal tissue in our body
fibrous tissue
synthesized within the body: Melanin, lipofuscin, hemoglobin, hemosiderin, bilirubin, etc
endogenous pigments
are formed outside the body: Carbon, soot, coal dust, silica, other environmental dusts, carotenoid, tetracycline, etc
exogenous pigments
the general term used for any organic and inorganic dust inhaled into and retained in the lung
inhalation of carbon
inhalation of silicon
cane pulp dust
cotten fiber dust
iron (as a result of hemorrhage)
most common exogenous pigment
ubiquitous carbon in the air
Yellow to orange yellow, fat-soluble pigments of plant origin, including β–carotene, the precursors of vitamin A
Normally occur in plasma and fat of horses, Jersey and Guernsey cattle, and sometimes dogs
carotenoid pigmentation
The pigments are not seen microscopically in routine pathologic sections b/c they are removed by alcohol; may obscure or confuse the dectection of icterus
carotenoid pigment
also called lipochrome pigments
carotenoid pigments
__________-based antibiotics administered during the teeth development will stain the teeth yellow or brown
also stains bone that is being laid down and has been used experimentally as a marker for that new bone
tetracycline abx
5 major endogenous
melanin, lipofuscin, hemoglobin, hemosiderin, bilirubin
A normal brown-black pigment in melanocytes, in epidermal cells, in pigmented epithelial cells of the eye, and occasionally in other tissues – protective mechanism (especially against UV light); Little pathologic significance other than need for recognition, depigmented skin and hair conditions, and melanoma
a circumscribed, nonpalpable spot <1cm in diameter in characterized by a change in color of skin
an acquired skin disease characterized by patches of unpigmented skin (often surrounded by a heavily pigmented border)
vitiligo (think mercy's nose)
a general lack of melanin due to a lack of tyrosinase. The affected animal is called albino
Cu deficiency in cattle and sheep can lead to ____ _ ___
defect in melaninogenesis
An insoluble pigment, aka lipochrome, wear-and-tear pigment or aging pigment; Composed of polymers of lipids and phospholipids complexed with protein; Derived through lipid peroxidation of polyunsaturated lipids of subcellular membrane in the lysosome; Not injurious to the cell of its function; Gross – yellow, tan to brown discoloration of affected tissues, particularly intestine
The term _____ is sometimes used to designate the wear-and-tear pigments, e.g., lipofuscin, haemofuscin, ceroid.
More precisely, ________ are yellow pigments that seem to be identical to carotene and xanthophyll and are frequently found in the serum, skin, adrenal cortex, corpus luteum, and arteriosclerotic plaques, as well as in the liver, spleen, and adipose tissue
In tissue sections, a yellow-brown, finely granular intracytoplasmic, often perinuclear pigmen; Seen in cells undergoing slow, regressive changes and is particularly prominent in the myocardial cells and neurons of aging patients or patients with severe malnutrition and cancer cachexia; EM – highly electron dense, membranous structures
a variant of lipofuscin, acid-fast and autofuorescent
a group of several genetically distinct disorders in children and animals
Neuronal ceriod-lipofuscinosis
In the dog, vitamin E or Se deficiencies can lead to ________ of the smooth muscle of the intestine; Unsaturated fatty acid-rich diet can increase the amount of ________
lipofuscinosis; lipofuscin
Hemoglobin and Hemoglobin-derived pigments
hematogenous pigments
4 types of hemoglobin
oxyhemoglobin, unoxygenated Hb, methemoglobin, carboxyhemoglobin
5 types of hematogenous pigments
hemoglobin, hemosiderin, bilirubin, hematoidin, hematin
transports CO2, NO
globin molecules of Hb
transports O2
heme molecules of Hb
a tetrapyrrole porphyrin ring containing ferrous (Fe2+) iron
Hemoglobin with the heme iron changed from the ferrous to the ferric state (Fe3+)
____________ is often due to nitrates, nitrite, chlorate and acetaminophen toxicities, mostly from fertilizer and drugs. The blood is brown, chocolate color that would stay 4-6 hours after death.
CO attached Hb. Hb has a high affinity for CO. The blood is bright cherry red.
Also the blood superoxygenated with ______ toxicity is bright cherry red
RBC’s die after 120 days and go to spleen to be recycles. _____ is a protein that we want to get back.
O2 carrying pigment of rbc – responsible for the pink appearance of the body
oxygenated arterial blood – bright red is due to what
the venous blood is bright red as the arterial blood
cyanide poisoning
carboxyHb – cherry red blood
CO poisoning
MetHb – reddish-brown (chocolate brown) blood
nitrite poisoning
pink plasma, icteric tissue; Hb is excreted by the kidney, staining the kidney dark red to black and the urine red. Similar, but often less severe, change may result from myoglobinuria after the destruction of muscle
Hb released from severe intravascular hemolysis
A Hb-derived, Fe-containing yellow-brown granular pigment; a partially denatured from of ferritin that easily aggregates
~ 25% of the body’s total iron content is in an intracellular storage pool composed of _____ (normal) and ______ (abnormal)
ferritin; hemosiderin
a protein that stores iron and releases it in a controlled fashion
In local and systemic excess of iron, ferritin forms intracytoplasmic _______ granules
Iron is normally carried by specific transport these glycoproteins in plasma
Under normal conditions, small amount of ________ can be seen in macrophages of the bone marrow, spleen and liver, all actively engaged in RBC breakdown; Can be seen in hemorrhagic areas
in congestive heart failure, ______ is seen in alveolar macrophages; grossly a yellowish tan to brown color of the lung is seen in pulmonary __________
hemosiderin; hemosiderosis
Excessive accumulation of iron in parenchymal organs such as the liver and pancreas, either from a genetic defect causing excessive iron absorption (hereditary ________) or as consequence of parenteral administration of iron (secondary ______)
leaking of cells thur capillary
like to accumulate when there is a low oxygen level
stain specific for iron
prussian blue reaction
Major pigment in bile but is only present in a small about; bile is mostly water and bile acids/salts which don’t contain pigment
Normal breakdown product of the heme, thus contains no iron (basically take heme, remove iron and then straighten the molecule)
May accumulate in the blood or in tissues in hemolytic diseases, or in hepatic and cholestatic disease, causing jaundice (icterus)
A green-brown to yellow-brown pigment in tissue sections
mixed with bilirubin to make water soluble
glucuronic acid
before bilirubin, heme is broken down into what
- Unconjugated hyperbilirubinemia (Crigler–Najjar syndrome type I) results from an autosomal recessive inherited deficiency of hepatic __________.
UDP-glucuronosyltransferase (UGT) 1A1 activity
6 mechanisms leading to icterus
Excess production of bilirubin (hemolysis); Reduced uptake of bilirubin from the plasma by hepatocytes; Impaired or absent conjugation in hepatocytes, often a inherited abnormality as in Gunn rat; Hepatic necrosis disrupting the wall of the bile canaliculus; Decreased excretion of conjugated bilirubin by the hepatocytes into the bile canaliculus;
Reduced flow of bile from liver to the intestine
icterus that is usually associated with intravascular hemolysis
hemolytic or prehepatic
3 types of icterus
Hemolytic (Prehepatic); hepatic; Posthepatic (Obstructive, cholestatic)
5 steps in the mechanism of bilirubin metabolism and elimination
Bilirubin production from heme; Unconj bilirubin is bound to serum albumin and delivered to the liver; Hepatocellular uptake;
Glucuronidation in the ER;
Gut bacteria degrade it to colorless urobilinogens. The urobilinogens (stercobilin) and the residue of intact pigments are excreted in the feces, with some reabsorption and excretion into urine (urobilin).
Hepatocellular uptake of bilirubin. _________ in the endoplasmic reticulum generate bilirubin __________ and ____________, which are water soluble and readily excreted into bile.
glucuronidation; monoglucuronides; diglucuronides
Gut bacteria ________ the bilirubin and degrade it to colorless ________. The _________ (stercobilin) and the residue of intact pigments are excreted in the feces, with some reabsorption and excretion into urine (urobilin).
deconjugate; urobilinogens; urobilinogens
Bilirubin is usually only toxic to the kidney under _______ conditions.
erythrocyte parasite
a yellow-brown pigment seen occasionally at sites of previous hemorrhage, and is believed to be locally precipitated bilirubin
a derivative of hemoglobin produced in tissues fixed in improperly buffered formalin (referred to as formalin pigment). It resembles hemosiderin but usually can be seen to overlie cells instead of being in them
acid hematin
category of acid hematin also include _______ hematin
Pink teeth and red-brown urine. Their teeth exhibit a red purple fluorescence b/c of the deposition of porphyrins in the dentin. The urine is red-brown b/c of the excretion of large amounts of uroporphyrin I; animals may also have photosensitivity
Inherited congenital porphyria
Porphyria occurs in cattle and cats as an inherited defect in the synthesis of the normal heme pigment, _______, leading to an accumulation of photodynamic _________.
ferroprotoporphyrin; porphyrins
3 types of photosensitization
primary, secondary (hepatogenous), congenital (enzyme deficiency)
the color of bilirubin, hemoglobin
the color of MetHb
chocolate brown blood
color of hemosiderin
tan to brown
color of porphyria
pink to red-brown
excess or lack of blood
congestion, hemorrhage, ischemia, anemia
color of accumulation of WBCs
white (abcess, lymphoma)
examples of mesenchymal tissues
DWCT, fibrosarcoma, fat, bone,
examples of deposits
Ca, urates
pigments produced by organisms
pseudomonas, corynebacterium, phaeohyphomyces, etc.