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General Pathology > Lecture 2: Calcification > Flashcards

Lecture 2: Calcification Flashcards

1
Q

__ is the abnormal Ca deposition in damaged tissues intracellularly or extracellularly which may cause the functional loss of tissue (i.e. elasticity)

A

dystrophic calcification

intracellular = mitochondrial
extracellular = plasma membrane, elastic tissue, basement membrane
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2
Q

sequelae of dystrophic calcification: may be reorganized to form __

A

heterotopic bone

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3
Q

__ is acute necrosis of skeletal and cardiac m due to vitamin E and selenium deficiency

A

white muscle dz

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4
Q

__ is abnormal Ca deposition in tissue secondary to hypercalcemia

A

metastatic

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5
Q

Mechanisms that lead to hypercalcemia

A 
hypervitaminosis D
toxic plants 
primary hyperparathyroidism
nutritional secondary hyperparathyroidism
hypercalcemia of malignancy
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6
Q

What causes hypervitaminosis D (leads to hypercalcemia/dystrophic calcification)

A 
dietary supplementation 
plant toxicity (cestrum diurnum and solanum malacoxylon)
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7
Q

Mechanism of hypervitaminosis D

A

stimulates intestinal Ca absorption and renal tubular Ca reabsorption

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8
Q

Metastatic calcification is located in the

A

BVs, elastic fibers, basement membranes (lung, kidney, stomach, oral cavity)

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9
Q

Common BV for metastatic calcification via hypervitaminosis D

A

aorta

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10
Q

sequelae of metastatic calcification

A
  1. renal tubular dysfunction (nephrocalcinosis)
  2. aortic rupture (rare)
  3. lung (hypoxemia, decreased capacity)
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11
Q

special stain for calcification that stains it black

A

von kossa stain

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12
Q

what causes primary hyperparathyroidism

A

primary parathyroid adenoma produces elevated PTH (stimulates osteoclast activity to increase bone resportion = increased Ca = hypercalcemia)

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13
Q

what happens with nutritional secondary hyperparathyroidism

A

inadequate Ca intake = decreased serum Ca = increased PTH = bone resoprtion = hypercalcemia

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14
Q

what happens with renal secondary hyperparathyroidism (very common!)

A

renal dz = decreased tubular phosphate excretion = increased phosphate in serum leads to CaP ppt. Also, Renal interference with Vit D metabolism (abnormal absorption) = HYPOcalcemia which stimulates PTH secretion = bone resorption = HYPERcalcemia. Widespread tissue calcification.

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15
Q

Many neoplasms produce ___ that induces bone resporption and hypercalcemia (anal apocrine gland adenocarcinoma, lymphoma)

A

PTH related protein (PTHrP)

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16
Q

__ pigment is a lipid-protein complex made from membrane lipids that is known as the “wear and tear” pigment

A

lipofuscin/ceroid

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17
Q

vitamin E deficiency, stress, increased lipid peroxidation product, age, etc will have__ pigment in tissues commonly seen the heart, liver, and brain

A

lipofuscin/ceroid

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18
Q

Lipofuscin/ceriod pigment is intralysosomal, it forms lysosomes by __

A

autophagocytosis

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19
Q

see an increased amount of lipofuscin pigment in neurons with genetic autosomal recessive dz called __ (abnormal metabolism of phospholipid)

A

neuronal ceroid lipofuscinosis

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20
Q

special stains/features for lipofuscin/ceroid (stains brown with H&E)

A

acid fast stain (blue) and autofluorescence

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21
Q

__ occurs in vitamin E deficient dogs and is also known as “brown gut dz”

A

Intestinal lipofuscinosis (lipofuscin/ceriod)

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22
Q

brown gut dz in dogs is due to increased membrane __ and accumulation of __ in intestinal smooth m.

A

lipid peroxidation, lipofuscin

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23
Q

Cats with vitamin E deficency do not get brown gut dz but have

A

fat necrosis in abdominal cavity

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24
Q

__ and __ pigments are derived from hemoglobin

A

hemosiderin and bilirubin

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25
Q

__ is derived from Hb when RBCs are phagocytosed and degraded intracellularly

A

hemosiderin

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26
Q

hemosiderin is normal in mononuclear phagocytes in the __, __, __

A

BM, spleen, liver

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27
Q

There is excess hemosiderin with __, __, __

A

hemorrhage/congestion, increased diet Fe, Hemolytic anemia

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28
Q

hemosiderin is usually not __ unless there is too much free ferrous iron (not bound) and the fenton rxn occurs making free radicals.

29
Q

When Fe is freed from Hb the body binds it to __ protein so it is less reactive and less likely to make free radicals (fenton rxn)

A

apoferritin/ferritin

30
Q

__ is a pathologic disorder of Fe metabolism

A

hemochromatosis

31
Q

hemosiderosis is seen with __ due to increased hydrostatic pressure in the lungs and RBC leak into alveoli where macs phagocytize them (brown macs)

A

chronic left heart failure

32
Q

special stain for hemosiderin that stains Fe dark blue

A

prussian blue (perls iron stain)

33
Q

how is hemosiderin made by macrophages phagocytizing RBC

A

macrophage breaks down RBC and Fe is bound to apoferritin making granular pigment (hemosiderin) in mac

34
Q

__ is a porphyrin (heme) ring of hemoglobin and other sources

35
Q

bilirubin is conjugated in the __ and excreted in the __

A

liver, bile

36
Q

clinical __ is seen when plasma bilirubin is >2-3mg/dl

37
Q

__ is toxic, cannot be excreted in the urine (bound to Albumin)

A

unconjugated bilirubin

38
Q

__ has low toxicity and can be excreted in the urine

A

conjugated bilirubin

39
Q

RBC are broken down into __ and __

A

ferrous iron and unconjugated bilirubin

40
Q

unconjugated bilirubin is taken up by the __ where it is conjugated and excreted to the bile duct for transportation to the __

A

hepatocyte, intestine (reabsorption and/or excretion via kidney)

41
Q

5 things that can cause hyperbilirubinemia/icterus/jaundice

A
  1. increased heme breakdown (anemai, hemorrhage)
  2. decreased hepatic uptake (drugs, dz)
  3. impaired conjugation (neonate, dz)
  4. impaired intra-hepatic excretion (cirrhosis, drugs)
  5. bile duct obstruction (inflamm, parasites, neoplasm, fb)
42
Q

Melanin pigment is formed by oxidation of __

43
Q

special stain for melanin that stains it black

A

fontana masson (argentaffin stain)

44
Q

some animals have normally occurring __in their lungs, heart, aorta, brain (sheep, pigs, etc)

45
Q

melanosis is common/normal in __

A

black-faced sheep breeds

46
Q

__ occurs when liver accumulates excess fat, turns yellow, and has a greasy consistency. When placed in water the liver will float and histologically hepatocytes will have “holes”

A

lipidosis, fatty change, steatosis

47
Q

Cats develop __ frequently due to too much FA to liver which is converted into triglycerides. Difficult to manage medically.

A

sever lipidosis

48
Q

Normally fat is processed by the liver via __ entering the cell and being converted into ___ by acetate and glycerophosphate. These TG must be bound to apoprotein to make __ that can leave the cell.

A

Free FA, triglycerides, lipoproteins

49
Q

if a dz or toxin affects protein synthesis what happens to the fat in the hepatocyte?

A

Steatitis - lipid gets trapped, TG need to be protein bound to exit the cell.

50
Q

lipidosis occurs normally during __

A

late pregnancy, lactation

51
Q

5 pathologic causes of lipidosis

A
  1. increased synthesis of FA, TG
  2. increased lipolysis and uptake of free FA
  3. decreased FA oxidation
  4. decreased Apoprotein synthesis
  5. decreased lipoprotein excretion
52
Q

___ is the accumulation of abnormal proteinaceous substance from several protein sources iwth eosinophilic staining that accumulates between cells and has beta pleated sheets

A

amyloidosis

53
Q

4 characteristics defining amyloid

A
  1. Abnormal proteinaceous substance
  2. Deposited extracellularly
  3. Results in organ dysfunction
  4. Derived from different proteins
54
Q

__ form crystals in the tissue (seen in renal granular amyloidosis) which can be stained with __

A

Amyloid Beta pleated sheets, congo red stain and polarized light (birefringence)

55
Q

2 Special stains for amyloidosis

A

Microscopically: Congo red - stains amyloid red (and polarized light for birefringence - yellow refraction)

Grossly: Lugol’s iodine and dilute sulfuric acid treatment (black) - used to see amyloid grossly (i.e. Dots in kidney)

H&E stains eosinophilic

56
Q

Amyloid more common in people/primates, occurs in vet med but it is less important

A

Primary Amyloid:AL - Ig light chains

57
Q

Most common form of amylodosis in animals that causes clinical disease

A

Secondaryr amyolid: AA - chronic inflammation, SAA precursor

58
Q

Amylodiosis that commonly is seen in cats caused by a partial degradation of protein in the pancreas leads to amyloid deposits in pancreatic islets (beta cell damage = diabetes)

A

Endocrine Amyloid

Islet amyloid polypeptide (IAPP) precursor secreted by beta cells with insulin, abormal synthesis/process/degradation = amylodosis.

59
Q

Amyloidosis associated with alzheimer’s dz in people described in dogs (human models)

A

Beta amyloid: senile plaques (APP amyloid precursor protein)

60
Q

Commonly seen in horses is amylodosis of apolipoprotein AI and AII

A

Aging associated amyloid

61
Q

How does secondary amyloidosis arise

A

Chronic inflammation - macrophage activate - IL and TNF secreted - Hepatocytes make SAA protein (serum amyloid A) - LIMITED PROTEOLYSIS occurs = AA

62
Q

How do you monitor secondary amylodosis

A

Via the acute phase reactant protein, SAA - serum amyloid A production

63
Q

Animal that develop dz from secondary amyloidosis is due to

A

BOTH limited proteolysis AND abundant production of SAA via the liver

64
Q

Primary amyloidosis is caused by

A

Ig light chains and limited proteolysis

65
Q

Consequences of amyloidosis in the kidney

A

Protein losing nephropathy

66
Q

Consequences of amyloidosis in the pancrease

A

Type 2 diabetes mellitus

67
Q

Consequences of amyloidosis in the GI tract

A

Impaired absorption

68
Q

Consequences of amyloidosis in the brain

A

Reduced cognitive performance/dementia (alzheimer’s in people)

69
Q

What organs are consequences more commonly seen in people

A

Liver (atropy, failure)
Heart (arrhythmia, failure)
Brain (dementia)

General Pathology (14 decks)

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