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Concepts in Pathology and Tissue Morphology > Intracellular Accumulations and Pathologic Calcification > Flashcards

Intracellular Accumulations and Pathologic Calcification Flashcards

1
Q

what mechanism of intracellular accumulation occurs in fatty liver/steatosis?

A

abnormal metabolism

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2
Q

what occurs in abnormal metabolism that results in intracellular accumulations?

A

inadequate removal of a normal substance secondary to defects in mechanisms of packaging and transport

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3
Q

all major lipids can accumulate in cells. what are they and examples

A
  • triglycerides (eg steatosis)
  • cholesterol/cholesterol esters (eg atherosclerosis)
  • phospholipids (eg myelin figures in necrotic cells)
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4
Q

what is steatosis

A

accumulation of triglycerides within parenchymal cells (can be liver, heart, muscle, kidneys)

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5
Q

what is the main organ involved in fat metabolism

A

liver

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6
Q

is steatosis reversible?

A

up to a point, otherwise irreversible damage (ie cirrhosis of liver)

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7
Q

what is an important use of cholesterol

A

synthesis of cell membranes

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8
Q

what is atherosclerosis?

A

a gross manifestation of atherosclerotic plaques -> smooth muscle cells and macrophages in surface/wall of arteries filled with lipid vacuoles (mostly cholesterol and cholesterol esters)

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9
Q

atheromas have a yellow appearance, what causes this?

A

aggregates of foam cells in surface/wall of vessels

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10
Q

what are foam cells?

A

macrophages that have ingested cholesterol

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11
Q

what is a “cholesterol cleft”

A

the histologic appearance of extracellular cholesterol esters that have crystallized as long needles

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12
Q

what mechanism of intracellular accumulation occurs in atherosclerosis?

A

abnormal metabolism

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13
Q

a xanthoma can occur in a hyperlipidemic or non-hyperlipidemic state. what is a xanthoma

A

groups of foamy macrophages found in the CT of skin and in tendons

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14
Q

what is cholesterolosis?

A

focal accumulation of cholesterol containing macrophages in lamina propria. most often affects gallbladder

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15
Q

what mechanism of intracellular accumulation occurs in renal tubule resorption droplets?

A

abnormal metabolism

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16
Q

when are renal tubule resorption droplets seen?

A
  • in kidney conditions with protein loss in the urine (proteinuria)
  • in heavy proteinuria -> increased resorption of proteins into vesicles
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17
Q

what do protein droplets looks like histologically

A

pink hyaline droplets within cytoplasm of proximal tubular cells

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18
Q

renal tubule resorption droplets reversible or irreversible?

A

reversible

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19
Q

what is a russell body

A

a large eosinophilic cytoplasmic protein droplet that can be seen in some plasma cells actively synthesizing immunoglobulins (ie areas of chronic inflammation or plasm cell neoplasms)

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20
Q

excessive deposits of glycogen may be seen with

A

abnormal glucose or glycogen metabolism

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21
Q

what is the histologic appearance of glycogen deposits?

A

it dissolves in aqueous fixatives -> appears clear

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22
Q

diabetes is the most important example of a disorders of glucose metabolism. what can be seen here as far as intracellular accumulations?

A

glycogen deposits in renal tubular cells, liver, and heart cells

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23
Q

glycogen storage diseases (glycogenoses) are enzymatic defects in the synthesis or breakdown of glycogen. (eg pompe disease and von gierke disease) what happens?

A

massive accumulation of glycogen -> cell injury and cell death

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24
Q

what occurs when there is a defect in protein folding/transport that causes intracellular accumulations?

A

•accumulation of endogenous substance due to defects in folding, packaging, or transport of proteins (can be genetic or acquired)

25
Q

mutated forms of alpha 1 anti-trypsin can cause

A

intracellular accumulations due to defective folding/transport

26
Q

what happens at the cellular level in mutated alpha 1 anti-trypsin?

A

mutation slows down the folding -> build up of partially folded intermediates aggregate in ER of liver cells -> not secreted

27
Q

what happens at the systemic level with mutated alpha 1 anti-trypsin?

A
  • deficiency of circulating enzyme causes emphysema of lung

* may also be damage from ER stress

28
Q

what occurs when there is lack of an enzyme that causes intracellular accumulations?

A

•failure to degrade a metabolite due to inherited enzyme deficiency

29
Q

what is niemann-pick disease (type c)

A

a lysosomal storage disease with a mutation affecting the enzyme involved in trafficking cholesterol -> accumulation of cholesterol in multiple organs

30
Q

what is the mechanism involved in intracellular accumulations found in niemann-pick disease type c

A

lack of an enzyme

31
Q

what occurs with ingestion of indigestible materials that results in intracellular accumulations

A
  • deposition and accumulation of abnormal substance

* occurs when cell does not have enzymatic machinery to degrade the substance or ability to transport it to other sites

32
Q

what is the mechanism of carbon or silica accumulation?

A

ingestion of indigestible materials

33
Q

what is anthracosis

A

the blackening of lung parenchyma and node tissues caused by accumulation of inhaled carbon

34
Q

what is the most common exogenous pigment that can be accumulated in the body

A

coal dust

35
Q

how does carbon accumulation occur in lungs

A

inhalation -> alveolar macorphages -> transported through lymphatic channels to regional (tracheo-bronchial) lymph nodes

36
Q

lipofuscin or lipochrome is sometimes called the “wear and tear” pigment and has a brown-yellow appearance. where can it accumulate

A
  • cells undergoing slow regressive change

* prominent in liver and heart of aging people or patients with severe malnutrition/cachexia

37
Q

lipofuscin is considered an endogenous pigment and is not harmful to cells, but its accumulation might indicate that a cell has been exposed to

A

free radical injury

38
Q

what does lipofuscin pigment look like histologically

A
  • yellow brown
  • finely granular
  • cytoplasmic, often perinuclear
39
Q

how is melanin formed

A

when tyrosinase catalyzed the oxidation of tyrosine to dihydroxyphenylalanine in melanocytes

40
Q

hemosiderin is an endogenous hemoglobin derived pigment. what causes it to form

A

condensation of excess ferritin deposition

41
Q

when can hemosiderin deposition be seen with normal iron breakdown

A

in sites where there is red blood cell breakdown (bone marrow, spleen, liver)

42
Q

in local excess of iron breakdown (ie hemorrhage into tissues -> bruise) macrophages break down blood. what causes the multicolors or resorbing bruise?

A
  • removal of iron -> ferritin -> hemosiderin

* also parallel breakdown of heme moiety (biliverdin=”green bile”, bilirubin=”red bile”)

43
Q

what is hemosiderosis

A

in systemic overload of iron -> hemosiderin can be deposited in many tissues

44
Q

what are the 3 main causes of hemosiderosis?

A

hemachromatosis, hemolytic anemias, and repeated blood transfusions

45
Q

what happens in hemachromatosis?

A

an inborn error of metabolism -> excessive absorption of dietary iron -> excessive deposition of hemosiderin

46
Q

what happens in hemolytic anemias

A

premature lysis of red blood cells -> release of abnormal quantities of iron -> excessive hemosiderin deposition

47
Q

accumulation is reversible in many cases if the overload can be stopped or controlled (eg early atherosclerosis or steatosis). in what cases are accumulations often not reversible?

A
  • inherited storage disorders where accumulation is progressive
  • overload -> cell injury -> may lead to death of cells, tissue, and patient
48
Q

what is dystrophic calcification

A
  • pathologic deposition of calcium locally in dying/abnormal tissue
  • typically calcium metabolism is normal
49
Q

what is metastatic calcification

A
  • pathologic deposits of calcium in otherwise normal tissues

* usually associated with hypercalcemia, some abnormality in calcium metabolism

50
Q

what is the gross appearance of calcification?

A

fine white granules that may be clumped and gritty to touch or cut

51
Q

histologic appearance of calcification

A
  • basophilic
  • amorphous granular
  • may be clumped
  • can be extracellular/intracellular/both
52
Q

what are psammoma bodies

A
  • can be seen with necrotic cells that cause calcium deposition
  • subsequent deposition of additional layers -> lamellated appearance
53
Q

where are psammoma bodies often seen

A

in tumors with a papillary morphology (ie serous ovarian tumor)

54
Q

what are asbestos bodies

A
  • found in lung
  • deposition of calcium and iron salts
  • beaded dumbbell appearance
55
Q

increased secretion of parathyroid hormone (PTH), which

can be due to parathyroid tumors, can cause

A

bone resorption -> hypercalcemia -> metastatic calcification

56
Q

resorption of bone (ie myeloma, leukemia, extensive skeletal metastases, paget’s disease, immobilization) can cause

A

hypercalcemia -> metastatic calcification

57
Q

vitamin d related disorders such as vitamin d intoxication or sarcoidosis can cause

A

hypercalcemia -> metastatic calcification

58
Q

renal failure can lead to retention of phosphate -> hyperparathyroidism ->

A

hypercalcemia -> metastatic calcification

59
Q

metastatic calcification can occur throughout the body, but some sites are predisposed to calcification. what are they and why

A
  • gastric mucosa, kidneys, lungs

* because they secrete acid -> have an internal alkaline compartment that is predisposed

Concepts in Pathology and Tissue Morphology (10 decks)

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