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VETM 342 - Pathologic Basis of Disease > Cellular Accumulations > Flashcards

Cellular Accumulations Flashcards

1
Q

two types of cellular accumulations

A

endogenous and exogenous

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2
Q

3 categories of cell accumulations

A
  1. normal cell constituent in excess (fats, carbs, protein)
  2. normal/abnormal substance due to genetic or acquired defects in cell processes
  3. a pigment
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3
Q

how does a normal cell constituent accumulate in excess?

A

endogenous substance produced at normal or increased rate and rate of metabolism is unable to remove it

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4
Q

3 common intracellular accumulations

A
  1. hepatic lipidosis
  2. glycogen in hepatocytes or muscles
  3. viral inclusions (aka viral proteins)
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5
Q

what is hepatic lipidosis and what is its pathogenesis?

A

= accumulations of triglycerides or other lipid metabolites (like neutral fats or cholesterol) in hepatocytes

pathogenesis: fat metabolism is impaired

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6
Q

why does lipidosis commonly manifest in the liver?

A

liver is most central organ in lipid metabolism and the clinical manifestation of cellular lipid accumulation is usually related to lipid function

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7
Q

where do we commonly see hepatic lipidosis in animals?

A

in animals where there is an increased demand for energy

found in obesity, starvation, diabetes mellitus, idiopathic in cats and cattle

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8
Q

gross changes associated with hepatic lipidosis

A
  1. enlarged
  2. yellow, soft, friable
  3. greasy texture
  4. broad, rounded edges
  5. floats in formalin
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9
Q

microscopic changes associated with hepatic lipidosis

A

highly vacuolated cytoplasm, can have sharply delineated borders

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10
Q

what is glycogen accumulation and what is its pathogenesis?

A

excessive amounts of glycogen, caused by an abnormal glucose or glycogen metabolism

can be a side effect of diabetes mellitus, Cushing’s disease, hyperglycemia, and can result from an animal being given too much steroids

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11
Q

give an example of a steroid-induced glycogen accumulation.

A

steroid-induced hepatopathy

  • hepatocytes are highly permeable to glucose
  • in steroid-induced hepatopathy we have a massive storage of glycogen
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12
Q

ways to distinguish hepatic lipidosis from steroid-induced hepatopathy

A

steroid-induced hepatopathy yields a swollen and pale liver, which is waxy as opposed to greasy, does not appear yellow like in hepatic lipidosis

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13
Q

microscopic changes associated with glycogen accumulation

A
  • swelling and vacuolation of hepatocytes
  • vacuoles are clear (like intracellular fat)
  • vacuoles are more irregular with less distinct outlines (rarefaction)
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14
Q

what are viral inclusions?

A

these are accumulations of viral proteins; found in the nucleus, cytoplasm, or both

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15
Q

how do we use the presence of viral inclusions?

A

diagnostically these can confirm specific viral diseases

ex. herpesvirus, adenovirus, parvoviruses = intranuclear inclusions
ex. rabies = Negri bodies (in the cytoplasm of neurons)
ex. canine distemper = both cytoplasmic and intranuclear inclusions

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16
Q

what is ab/normal substance from genetic/acquired defects that we see? include pathogenesis.

A

diseases that occur when a certain enzyme is deficient. this missing enzyme usually breaks down certain products so there is a resulting accumulation of complex substrates

the buildup of these complex substrates cannot be exported or broken down further

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17
Q

mucopolysaccharidosis (MPS), what is it and what does it cause?

A

inherited metabolic disorders that result from a deficiency of lysosomal enzymes needed for catabolism of glycosaminoglycans (GAGs)

the buildup of GAGs causes progressive/irreversible cell damage affecting growth, morphology, mobility, organ function, neurodevelopment

MPS type 6 - accumulations in the joints which impair movement

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18
Q

MPS - histo characteristics

A

neutrophils have pink granules accumulating (which are GAGs)

muscle cells contain abundant cytoplasmic vacuoles

19
Q

two examples of extracellular accumulations

A

amyloid

gout

20
Q

what is amyloid and how is it formed?

A

amyloid is a pathologic proteinaceous substance deposited in extracellular space of various tissues

it is formed by the misfolding of soluble and functional peptides/proteins, which converts them into insoluble, rigid and non-functional aggregates

when misfolded, function is lost and the tissue containing this deposit is damaged (causes compression atrophy in adjacent/parenchymal cells)

21
Q

there are two types of amyloidosis, localized and systemic. what are three examples of systemic (multi-organ) amyloidosis?

A
  1. primary amyloidosis (AL amyloid light chains)
  2. secondary amyloidosis (AA)
  3. hereditary/Familiar (AA) amyloidosis
22
Q

what is primary / AL amyloidosis? where can it show up?

A

these affect the light chains of immunoglobulin molecules, which are produced in excess in neoplastic plasma cells (in B cell lymphoproliferative disorders), misfold and become AL proteins which build up in tissues like urine or serum

key distinction here is that it can show up inside and outside cells

23
Q

what is secondary amyloidosis (AA)? what organs does it involve?

A

reactive form of systemic amyloidosis; caused by the abundance and buildup of serum amyloid A (“SAA” an acute-phase protein) from chronic inflammation

continual increase in SAA, and a small proportion will spontaneously misfold and accumulate in tissues

can involve kidneys, liver, spleen, lymph nodes

  • most common in domestic animals *
24
Q

what is the key distinguishing feature when observing AA amyloidosis? Gross/micro

A

Grossly: pale, beige, firm, waxy and UNIFORMLY DISTENDED

Microscopically: can see buildup of eosinophilic, hyaline material (aka amyloid)

25
Q

what is gout?

A

deposition of sodium urate crystals in the tissues

occurs when there is abnormal purine metabolism, resulting in higher concentrations of uric acid

can become chronic

26
Q

what can cause the increase in uric acid?

A
  • protein-rich diet
  • vitamin A deficiency
  • renal injury or disease
  • severe dehydration (and less uric acid is cleared)
27
Q

what are the two forms of gout?

A

visceral (on serosa, like pericardium, kidneys, liver, spleen) - usually from kidney failure

articular (deposits in/around joints) - usually diet-related or hereditary

28
Q

what are tophi?

A

aggregations of sodium urate crystals, which appear as white nodules

29
Q

what is pathologic calcification and what are the two forms?

A

= deposition of calcium salts in dead/dying/normal tissue

  1. Dystrophic Calcification
  2. Metastatic Calcification
30
Q

how does dystrophic calcification occur and what is its significance?

A

occurs where necrosis is; caused by the inability for dead/dying cells to regulate influx of calcium

because calcium is not regulated, it accumulates intracellularly

results in permanent change but is not an issue unless there is mechanical interference of function

this is NOT ASSOCIATED WITH HYPERCALCEMIA

31
Q

how does metastatic calcification occur and what are 4 common diseases that lead to it?

A

occurs in normal tissue/living tissue - increased number of calcium ions enter cells, which then precipitate within cells or interstitium

this IS ASSOCIATED WITH HYPERCALCEMIA

diseases that lead to it…

  1. increased PTH or PTH-related protein production
  2. bone destruction from primary/metastatic bone tumours
  3. vitamin D toxicosis
  4. renal failure/chronic kidney disease (CKD)
32
Q

what are the 2 types of pigments, with examples?

A

exogenous - from outside body; ex. carbon, carotenoids, tattoos
endogenous - from inside body; ex. melanin, hematogenous

33
Q

what is the most common exogenous pigment? how do you know that you have this accumulation?

A

carbon

  • enters through inhalation; accumulation in lung = anthracosis / black lung

Grossly: fine black foci (peribronchiolar deposits)
Micro: carbon is phagocytosed by macrophages, transported to peribronchial region; accumulates in interstitial tissues around airways

34
Q

what are tattoos?

A

pigments introduced into the dermis, which are phagocytosed by macrophages but remain within the dermis

does not invoke an inflammatory response

35
Q

what are carotenoids?

A
  • fat-soluble plant based pigments like beta-carotene (vit A precursor)
  • discolours fat to yellow-orange; common in fat of horses, some cattle and some dogs

do NOT confuse for icterus!

36
Q

what is melanin? what enzyme is crucial in its production?

A

melanin is an intracellular, brown/black pigment derived from tyrosine. its main function is to protect from solar UV light

requires copper-containing enzyme TYROSINASE to occur

37
Q

what are abnormal melanin pigmentation examples?

A

hyperpigmentation = chronic dermatitis, endocrine dermatopathies, neoplasms of melanocytes

hypopigmentation = albinism, from lack of tyrosinase; copper deficiency

38
Q

name three hematogenous pigments that can accumulate

A

hemoglobin
hemosiderin
bilirubin

39
Q

what do we see in accumulations of hemoglobin?

A

in intravascular hemolysis…

  • hemoglobin is released from the breakdown of RBCs
  • get pink/red plasma or serum (hemoglobinemia = Hb release)
  • get hematuria (red pee!)
40
Q

what do we see in accumulations of hemosiderin?

A

hemosiderin is formed from the lysis (breakdown) of erythrocytes

it represents stored iron from destroyed RBCs; accumulates within macrophages in spleen and bone marrow or hemorrhaged tissues

Grossly: tissues are light brown
Micro: yellow-brown (histo), green-black (cyto) granular intracellular pigment

41
Q

hemosiderosis vs hemochromatosis

A

hemosiderosis = mild/moderate hemosiderin accumulation, usually no damage

hemochromatosis = excessive hemosiderin accumulation, accompanied by cell damage

42
Q

bilirubin

A

yellow-brown or brown-green pigment that develops from Hb breakdown as macrophages process older RBCs

43
Q

what do we see in accumulations of bilirubin?

A

icterus! - tissue stains yellow from the imbalance between production and clearance of bilirubin

Grossly: diffuse yellow discoloration throughout body, especially in adipose tissue and mucous membranes
Micro: see “bile casts” - bilirubin in bile ducts/canaliculi

44
Q

3 causes of icterus:

A

pre-hepatic = from hemolysis

hepatic = hepatocellular swelling that compresses canaliculi, lesions compress bile ducts

post-hepatic = bile duct obstruction

VETM 342 - Pathologic Basis of Disease (3 decks)

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