Pneumoconiosis Flashcards

1
Q

Pneumoconiosis Definition

A

Diffuse lung disease caused by inhalation of inorganic dust.

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2
Q

Four Mineral Dusts

A

Asbestos

Beryllium

Coal

Silica

•Know your ABCs!

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3
Q

Factors Influencing the Development of Pneumoconiosis

A
  1. Amount of dust retained in the lung.
  2. Size and shape of the dust particles.
  3. Solubility and chemical reactivity of the dust particles.
  4. Presence of other irritants, such as cigarettes, or other diseases.
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4
Q

Amount of dust retained in the lungs is determined by:

A
  • Concentration of dust in the ambient air.
  • Duration of exposure.
  • Effectiveness of clearance mechanisms
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5
Q

Defense Mechanisms of the Respiratory Tract

A
  1. Filtration and impaction in the upper respiratory tract.
  2. Cough.
  3. Mucociliary transport.
  4. Phagocytosis and transport by macrophages.
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6
Q

Coal Workers’ Pneumoconiosis - Definition

A

A chronic lung disease caused by accumulation of inhaled coal/carbon dust in the lung, accompanied by variable amounts of lung fibrosis.

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7
Q

CWP Pathogenesis

A

Although disease is clearly associated with increased exposure to and accumulation of inhaled coal dust, the pathogenesis of CWP is poorly understood. Fibrosis is probably caused by immunologic mechanisms, but the amount of coal retained in the lungs is of pivotal importance.

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8
Q

Simple Coal Workers’ Pneumoconiosis (CWP):

A

Small aggregates of coal dust-laden macrophages (coal macules) form in the region of terminal bronchioles and respiratory ducts.

  1. Little or no disturbance in ventilatory function; symptoms mild.
  2. Little to no fibrosis.
  3. Often associated with a form of centriacinar emphysema.
  4. May progress to fibrous nodules with dust (nodular CWP); still little functional impairment.
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9
Q

Complicated Coal Workers’ Pneumoconiosis:

A
  1. Also called “Progressive Massive Fibrosis” (PMF), although PMF is not unique to CWP and can occur with other pneumoconioses, too.
  2. Bulky nodules of fibrous tissue greater than 2 cm, with large amounts of black dust, typically more severe in upper lobes.
  3. May cause severe pulmonary symptoms and cor pulmonale (right heart failure).
  4. Patients are susceptible to secondary tuberculosis infection in the areas of nodular scarring.
  5. Less than 10% of patients with simple CWP progress to PMF.
  6. In coal workers who also have rheumatoid arthritis, may result in Caplan syndrome: combined PMF and rheumatoid lesions in the lung.
  7. In the absence of smoking, no increased risk for lung cancer has been observed in CWP.
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10
Q

Anthracosis

A
  • “Anthracosis” is a term that literally means black dust accumulation in the lungs, and occurs in miners and non-miners alike.
  • It is not a disease, but a consequence of living, particularly in urban areas with air pollution. However, there is a spectrum of alterations that occur as an individual is exposed to increasing amounts of carbon-containing dust, ranging from anthracosis in the beginning, to simple (macular) CWP, CWP with early fibrosis (nodular CWP), and finally to full-blown PMF.
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11
Q

Silicosis Definition

A
  • A chronic lung disease caused by accumulation of inhaled silica dust in the lung, accompanied by variable amounts of lung fibrosis.
  • Approximately 20% of the earth’s crust is silica (silicon dioxide). Thus, any mining activity exposes one to particles of crystalline silica unless precautions are taken. Numerous other dusty occupations can also expose workers to silica, especially sandblasting, stone polishing, concrete mixing, demolition, foundry work, rock drilling, and many others.
  • Silicosis is the most prevalent chronic occupational disease in the world.
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12
Q

Silicosis Pathogenesis

A

The macrophage plays a pivotal role in the development of fibrosis. Silica is chemically active; SiOH groups interact with cell membranes. Free radicals are generated. Phagocytosed silica particles trigger release of various enzymes as well as chemical mediators that cause the accumulation of other chronic inflammatory cells. Interleukins, TNF, and fibroblast growth factors are involved.

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13
Q

Nodular (Chronic) Silicosis:

A
  1. 1-5 mm parenchymal “silicotic nodules” consisting of layers of relatively acellular fibrous tissue mixed with silica crystals; in upper lobes of lungs mostly.
  2. Lymph nodes are frequently also involved by silicotic nodules.
  3. Development insidious over many years of exposure.
  4. Often few symptoms, since most of the lung is not involved.
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14
Q

Complicated (Conglomerate) Silicosis:

A
  1. Coalescence of smaller silica nodules into large fibrous masses in the lungs.
  2. Associated with respiratory impairment, right heart failure, and more severe symptoms.
  3. Like PMF in the setting of coal workers’ pneumoconiosis, PMF in silicosis also predisposes patients to secondary infection with tuberculosis (“silicotuberculosis”).
  4. Like PMF in CWP, workers with rheumatoid arthritis can develop Caplan syndrome (combined PMF and rheumatoid lesions).
  5. Risk of lung cancer is controversial.
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15
Q

What is asbestos?

A

•The term asbestos is used for a family of related silicate minerals that form long, thin fibrous crystals and have excellent fire-retardant and insulation properties. For these reasons, asbestos was used historically in numerous industrial applications and products, such as shipbuilding, fireproofing, insulation, fireproof clothing, fire blankets, brake pads, plaster, popcorn ceilings, vinyl floor tiles, and many others. Visible fibers are composed of innumerable microscopic fibrils that are released by abrasion and other manipulation. Six distinct types are recognized, in two major groups:

  1. Serpentine
  2. Amphibole
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16
Q

Serpentine (white) asbestos

A
  • curly and flexible fibers
  • Chrysotile.
17
Q

Amphibole (brown) asbestos

A
  • straight, stiff, and brittle fibers
  • Crocidolite, amosite, tremolite, anthophyllite, actinolite.
18
Q

Types of Asbestos

A
  • These types vary in risk for carcinogenicity and fibrogenicity, with amphibole asbestos being much more pathogenic than serpentine asbestos. Serpientine fibers are more soluble and are more easily removed by macrophages.
  • Nevertheless, ALL types of asbestos can cause asbestos-related disease. Asbestos is everywhere. It is present in your lungs right now, in the air you breathe, and in the water you drink.
  • Asbestos-associated diseases are a consequence of inhaling concentrations of asbestos significantly above background levels.
19
Q

Exposure to Asbestos

A
  1. Interstitial fibrosis of the lungs (asbestosis).
  2. Pleuritis and pleural effusions.
  3. Fibrous pleural plaques.
  4. Diffuse malignant mesothelioma.
  5. Primary lung carcinoma.
  6. Cancer in other organs.
20
Q

Asbestos Pathogenesis

A
  1. Despite the long narrow shape of the fibers (up to 50-80 microns long), they are inhaled deeply into the lung because airflow causes them to become aligned in parallel with the bronchial lumen during inspiration.
  2. Asbestos fibers become coated with iron and proteins and are then called “asbestos bodies”.
  3. Lung parenchyma is injured because of release of various chemical mediators as the asbestos fibers are phagocytized.
  4. Specific mechanisms underlying development of asbestos-related diseases are still poorly understood.
21
Q

Asbestosis

A

•Asbestosis is diffuse interstitial fibrosis (scarring) of the lungs caused by asbestos exposure. Unlike CWP and silicosis, asbestosis does NOT result in fibrotic nodules or masses, but causes diffuse fibrosis instead for unknown reasons. The disease begins around respiratory bronchioles, where dust usually settles out. Health consequences are the same as for other diffuse interstitial diseases.

*lung fibrosis due to asbestos = asbestosis*

22
Q

Pleural Plaques

A
  1. Thick deposits of fibrous tissue on surface of parietal pleura, especially the diaphragmatic pleura, caused by asbestos exposure, and often calcified

. 2. Don’t contain asbestos bodies!

  1. A very good marker for asbestos exposure, but not entirely specific, as pleural plaques can rarely occur in non-exposed persons.
23
Q

Cancer Related to Asbestos Exposure

A

Asbestos increases risk for development of several types of malignancy, including diffuse malignant mesothelioma, lung carcinoma, and other cancers. An estimated 50-80% of all mesotheliomas of the pleura are due to asbestos exposure, and the risk of mesothelioma is increased by more than 1000-fold in individuals exposed to asbestos. Some peritoneal mesotheliomas are also due to asbestos exposure, but it is unclear how the asbestos fibers stimulate neoplastic transformation of the normal mesothelium in these two sites. Asbestos exposure also increases the risk for lung carcinoma five-fold, and potentiates the effects of smoking to further increase this risk.

24
Q

Latency in the Development of Asbestos-Associated Disease:

A
  1. Asbestosis and lung carcinoma develop in patients that are chronically exposed to fairly large amounts of asbestos fibers. Typically, they have been exposed for several years before developing asbestosis or lung carcinoma.
  2. Pleural mesothelioma tends to develop 25-40 years after asbestos exposure. The initial exposure may be quite short, perhaps only a few months. A classic history is lining the holds of ships with asbestos fireproofing material during World War II, with the development of mesothelioma decades later.
25
Q

Berylliosis Definition

A

A chronic lung disease caused by accumulation of inhaled beryllium dust in the lung, accompanied by variable degrees of granulomatous inflammation in the lung.

26
Q

Berylliosis

A
  1. Produced by exposure to inhaled metallic beryllium or berylliumcontaining compounds.
  2. Exposure to beryllium dust may be hard to document. Beryllium is used in the fabrication of electrical equipment and is part of alloys that may be ground or polished.
  3. Berylliosis causes granulomatous disease in the lungs that appears virtually identical to sarcoidosis.
  4. Occasionally granulomas are also found in regional lymph nodes and viscera.
  5. The granulomatous response represents a type IV hypersensitivity response, not one directly related to the amount of beryllium inhaled.
  6. An increased risk of lung cancer is likely.
27
Q
A

Asbestos Bodies

28
Q

Silicosis, Tuberculosis, and Lung Cancer

A
  • Increased incidence of tuberculosis in silicosis
  • Due to impaired macrophage function or socioeconomic factors
  • Mildly increased incidence of primary lung cancer with silicosis