Pigmentations, Calcifications and Gout Flashcards

1
Q

the most common exogenous pigment is ____

explain this

A

the most common exogenous pigment is carbon

  • aggregates of the pigment blacken the draining lymph nodes and pulmonary parenchyma (anthracosis)
  • phagocytosed by alveolar macrophages
  • in industry, often with other pollutants, i.e. silica, asbestos
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2
Q

describe tattooing

A
  • introduction of insoluble metallic and vegetable pigments into skin (dermis)
  • picked up by dermal macrophages
  • remains in the dermis for life
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3
Q

describe what is seen in the image

A

tattoo in the dermis of the skin (black pigments = tattoo)

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4
Q

describe melanin

A
  • endogenous pigment produced by melanocytes
  • once produced by the cells, it is stored in intracellular organelles called melanosomes
  • melanin has the function of acting as a protective barrier of our skin by absorbing potentially harmful UV light
  • although melanocytes are the only cells able to produce melanin, melanin once extruded by melanocytes can be accumulated by basal epithelial cells of the skin (freckles), by nevus cells (epidermis/dermis) or by dermal macrophages
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5
Q

describe what is seen in the image

A
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6
Q
A
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7
Q

describe lipofuscin (cause, storage, significance)

A
  • endogenous “wear and tear” pigment
  • result of free-radical induced break down of intracellular membranes
  • stored in lysosomes
  • not believed to interfere with cell function; hallmark of aging
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8
Q

describe what is seen in the image

A

lipofuscin accumulation in liver cells

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9
Q

describe bile and bilirubin

A
  • aqueous mixture of conjugated bilirubin, bile salts, phospholipids, cholesterol and electrolytes
  • bilirubin is a pigment derived from the breakdown of old RBCs
  • bile is visible when there is obstruction of the biliary ductal system, bile ducts or bile canaliculi
    • when obstruction occurs, some excess bilirubin in the circulation accumulates in the tissues
      • skin and conjunctiva become yellow = jaundice
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10
Q

describe hemosiderin

A
  • hemoglobin-derived granular pigment that is golden yellow to brown and accumulates in tissues with excess iron
  • hemosiderin pigment represents large aggregates of ferritin micelles
  • the iron can be identified with Prussian blue
  • excess deposition of hemosiderin = hemosiderosis; even more extensive accumulation of iron = hemochromatosis
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11
Q

describe 3 causes and symptoms of hemosiderosis/hemochromatosis

A
  • causes
    • excess intestinal absorption of Fe (hemochromatosis specifically)
    • excess RBC breakdown
    • transfusion
  • symptoms of hemochromatosis
    • bronze skin
    • diabetes mellitus
    • cirrhosis
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12
Q
A
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13
Q

describe the difference between the images

A
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14
Q

describe dystrophic calcification

A

occurs during cell injury/death

  • initiation of intracellular calcification occurs in the mt of dead or dying cells that have lost their ability to regulate intracellular calcium
    • after initiation, propagation of crystal formation occurs which is dependent on the concentration of Ca2+ and PO4- and the degree of collagenization (which enhances the rate of crystal growth)
  • calcification can develop in aging or damaged heart valves, resulting in severely compromised valve motion
  • normal serum Ca2+ levels
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15
Q
A
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16
Q

describe what is seen in the 2 images

A
17
Q

describe metastatic calcification

A

occurs in normal tissues

  • associated with hypercalcemia
    • increased secretion of PTH (due to primary parathyroid tumor or production of PTH-related protein by other malignant tumor)
    • vit. Dintoxification
    • renal failure –> secondary hyperparathyroidism
18
Q

describe gout and gouty arthritis

A
  • deposition of urate crystals in soft tissues and joints (tophi)
    • most commonly found in feet because of gravity
  • the end result is cytokine-mediated destruction of articular cartilage
  • caused by hyperuricemia
    • disorder of purine metabolism
    • age, genetic predisposition, heavy alc. consumption, obesity, certain drugs (thiazides)
19
Q

describe the pathogenesis of gout

A
20
Q

describe the process of inflammation in gout

A
21
Q

describe the classification of gout

A
  • primary gout (90% of cases)
    • unknown enzyme defect
    • HGPRT deficiency
  • secondary gout (10% of cases)
    • increased nucleic acid turnover
    • chronic renal disease
    • inborn errors of metabolism (HGPRT absence aka LH syndrome)
22
Q

describe the macroscopic vs microscopic appearance of gout

A
  • gross:
    • tophi
    • arthritis with destruction of cartilage
  • microscopic
    • tophi: crystals + inflammation
    • foreign body giant cells
23
Q

describe what is seen in the image

A
24
Q

describe what is seen in the image

A