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General Pathology (Fall 2014) > Lecture 4: Calcification & Amyloidosis > Flashcards

Lecture 4: Calcification & Amyloidosis Flashcards

1
Q

2 forms of pathologic calcification***

A

dystrophic and metastatic

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2
Q

dystrophic calcification***

A

abnormal calcium deposition in damaged tissue (response to local injury)

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3
Q

location, functional significance, and sequelae of dystrophic calcification***

A

1) location: intracellular: mitochondria; extracellular: phosphate-rich plasma membrane, elastic tissue, basement membrane
2) fx sig: loss of tissue function/elasticity
3) sequelae: can serve as focus for heterotopic bone form.

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4
Q

how can Vit. E/selenium deficiency lead to calcification?*

A

can cause necrosis of muscle, followed by dystrophic calcification

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5
Q

Von Kossa stain and calcium*

A

stains Ca black

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6
Q

metastatic calcification is caused by***

A

Abnormal Ca deposition in “normal tissues” secondary to hypercalcemia

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7
Q

6 mechanisms of metastatic calcification**

A
  • hypervitaminosis D
  • toxic plants
  • primary hyperparathyroidism
  • nutritional secondary hyperparathyroidism
  • renal secondary hyperparathyroidism
  • hypercalcemia of malignancy
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8
Q

primary locations where metastatic calcification is found**

A
  • blood vessels/elastic fibers/basement membranes of lung, kidney, stomach, oral cavity
  • aorta (ruminants)
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9
Q

fx. significance of metastatic calcification**

A

loss of tissue fx (elasticity)

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10
Q

sequelae of metastatic calcification**

A

renal tubular dysfunction (nephrocalcinosis)
aortic rupture
hypoxemia, decreased lung capacity

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11
Q

Hypervitaminosis D cause and action*

A
  • dietary supplementation or plant toxicity

- action: stimulates intestinal Ca absorption, renal tubular Ca reabsorption

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12
Q

Primary Hyperparathyroidism mech.*

A

parathyroid adenoma produces excess PTH –> increased osteoclast activity –> increased bone resorption –> Ca released from bone resorption causes hypercalcemia

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13
Q

Nutritional Secondary Hyperparathyroidism mech.*

A

Low Ca intake –> low serum Ca –> elevation of PTH –> increased bone resorption and hypercalcemia

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14
Q

Renal secondary hyperparathyroidism mechs.* (complex!)

A

renal dz –> decreased tubular phosphate excretion –> elevated phosphate complexes serum Ca –> renal interference with Vit. D metabolism –> hypocalcemia –> PTH stimulated –> increased bone resorption and hypercalcemia

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15
Q

Mech. of Hypercalcemia of Malignancy*

A

many neoplasms produce PTH related protein that induces bone resorption and hypercalcemia

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16
Q

Amyloidosis*

A

accum. of abnormal proteinaceous substance from several protein sources with eosinophilic staining properties that accumulates between cells and has beta-pleated sheet conformation

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17
Q

Clicker: Calcification in a renal infarct is most likely due to which mech? (dystrophic or metastatic)**

A

dystrophic

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18
Q

Clicker: Which of the following are mechs. of metastatic calcification? CCl4 toxicity, primary parathyroid tumor, and/or hypervitaminosis D**

A

primary PT tumor, Hypervitaminosis D

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19
Q

What does amyloid look like on H&E stain? Congo red stain?*

A

homogenously pink on H&E. Red on Congo red. Side note: Can also use polarized light to create birefringence

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20
Q

most common form of amyloidosis in animals***

A

secondary amyloidosis (primary in humans)

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21
Q

What is primary amyloidosis composed of?*

A

amyloid AL (immunoglobulin light chains)

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22
Q

What is secondary amyloidosis composed of?***

A

Amyloid AA (amyloid-associatied), aka serum amyloid A protein

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23
Q

What is endocrine amyloidosis composed of?*

A

(derived from hormones) CGRP and IAPP

24
Q

Clicker: The most common form of amyloidosis in animals is derived from:**

A

Serum Amyloid A protein

25
Q

what is the precursor to AA protein?*

A

SAA (serum amyloid A) protein

26
Q

Serum Amyloid A protein is produced in response to what type of stimuli?*

A

chronic inflammation

27
Q

TNF –> liver*

A

upregulates SAA protein production in liver cells –> AA protein formation

28
Q

consequences of amyloidosis on kidney*

A

protein-losing nephropathy

29
Q

consequences of amyloidosis on pancreas*

A

Type 2 diabetes mellitus

30
Q

consequences of amyloidosis on liver*

A

atrophy, failure

31
Q

consequences of amyloidosis on heart*

A

arrhythmias, failure

32
Q

consequences of amyloidosis on GI tract*

A

impairs absorption

33
Q

consequences of amyloidosis on Brain*

A

reduced cog. performance, dementia

34
Q

Hemosiderin is derived from:*

A

Hb (when RBCs are broken down)

35
Q

melanin is derived from:*

A

oxidation of tyrosine

36
Q

What is bilirubin composed of?*

A

porphyrin ring of Hb

37
Q

What is lipofuscin/ceroid composed of?*

A

lipid-protein complexes (a product of lipid peroxidation)

38
Q

What stain detects lipofuscin/ceroid?*

A

blue in acid fast stain, or brownish in H&E. It will also fluoresce under fluorescent light

39
Q

Lipofuscin accumulation increases with what deficiency?*

A

Vit. E

40
Q

Where does lipofuscin accumulate?*

A

in lysosomes. Common in heart, liver, brain, intestines

41
Q

Hemosiderin is normally bound to:*

A

apoferritin/ferritin

42
Q

Where is hemosiderin normally found?*

A

bone marrow, spleen, liver (within macrophages)

43
Q

What causes hemosiderin excess?*

A

hemorrhage/congestion, increased dietary iron, hemolytic anemia, etc.

44
Q

T or F: hemosiderin is usually not toxic*

A

T

45
Q

Hemochromatosis*

A

too much iron in the body

46
Q

Prussian blue stains iron what color?*

A

blue

47
Q

Bilirubin is conjugated in the ____ and excreted in the ___*

A

liver; bile

48
Q

bilirubin has what color discoloration assoc. with it?***

A

yellow (causes icterus/jaundice)

49
Q

Possible Causes of Hyperbilirubinemia (5)*

A
  • increased heme breakdown
  • decreased hepatic uptake
  • impaired conjugation
  • impaired intra-hepatic excretion
  • bile duct obstruction
50
Q

Fontana Masson stains what black?*

A

melanin

51
Q

lipidosis is aka:*

A

fatty change, steatosis

52
Q

Clicker: Vit. E deficiency and lipid peroxidation contributes to formation of which pigment?**

A

Lipofuscin

53
Q

Clicker: Which pigments can result in brown pigmentation of organs and cytoplasm?**

A

melanin, hemosiderin, lipofuscin

54
Q

Steps of free fatty acids entering liver –> lipoproteins exiting liver*

A

1) free fatty acids transported into liver, bind with glycophosphate to form triglycerides
2) triglycerides form lipoproteins under influence of apoprotein and exit liver

55
Q

How does protein metabolism related to lipidosis?*

A

need to have functional protein metabolism for triglycerides to form lipoproteins and exit the liver. Anything that depresses hepatic protein synthesis will usually result in increased lipid in the hepatocytes

General Pathology (Fall 2014) (6 decks)

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