pneumoconiosis Flashcards

1
Q

definition of pneumoconiosis

A

The pneumoconioses are a group of interstitial lung diseases, mostly of occupational origin, caused by the inhalation of mineral or metal dusts.

  • Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts.
  • Simple – Coalworker’s pneumoconiosis or silicosis (asymptomatic)
  • Complicated – a pneumoconiosis (progressive massive fibrosis) = loss of lung func
  • Asbestosis – a pneumoconiosis where diffuse parenchymal lung fibrosis occurs as a result of prolongued asbestos exposure
  • Caplan’s syndrome The association between rheumatoid arthritis, pneumoconiosis, and pulmonary rheumatoid nodules.
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2
Q

aetiology of pneumoconiosis

A
  • inhalation of particles of coal dust (1-3um) over 15-20yrs, silica or asbestos (two main types of fibre: white asbestos and blue asbestos or crocidolite, the latter is more toxic).
  • Silicosis – caused by inhalation of silica particles which are fibrogenic
    • A number of jobs may be associated with exposure, eg metal mining, stone quarrying, sandblasting, and pottery/ceramic manufacture.
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3
Q

RF of pneumoconiosis

A
  • Occupational exposure
    • Coal mining
    • Quarrying
    • Iron and steel foundries
    • Stone cutting
    • Sandblasting
    • Insulation industry
    • Plumbers
    • Ship builders
  • Risk depends on extent of exposure, size, shape of particles and individual suspeptibility
  • Smoking
  • TB
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4
Q

pathogenesis of pneumoconiosis

A

Coal worker’s

  • Coal particles ingested by macrophages – release they’re enzymes = fibrosis

Progressive massive fibrosis is due to progression of coal worker’s

Complicated disease

  • Large nodules in lung – dust particles (coal/silica) surrounded by layers of collagen and dying macrophages
  • Direct cytotoxicity by particles
  • Particle ingestion by macrophages results in activate and excessive free radical production = lipid peroxidation and cell injury
  • Proinflamm cytokines and GF from macrophags and epithelial cells stimulate fibrblast proliferation and eventual scarring

Asbestosis

  • Asbestos bodies consisting of fibres coated with an iron-containing protein are seen in fibrotic areas – especially in lung bases
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5
Q

epi of pneumoconiosis

A
  • Incidence increasing in developing countries
  • Disability and mortality from asbestos will be increasing over next 20-30yrs
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6
Q

sx of pneumoconiosis

A

Occupational history is important, there may be a long latency between disease exposure and expression.

Asymptomatic – found on routine CXR – simple coal or silica pneumoconiosis

Symptomatic

  • Insidious onset of SOB and dry cough
  • Black sputum – melanoptysis in coal worker’s
  • Workers exposed to asbestos may develop pleuritic chest pain from asbestos pleurisy

Progressive massive fibrosis

  • Progressive dyspnoea
  • Fibrosis
  • Cor pulmonale

Silicosis

  • Progressive dyspnoea
  • Increased incidence of TB
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7
Q

signs of pneumoconiosis

A

May be normal

Decreased breath sounds in coalworker’s pneumoconiosis or silicosis.

In coal worker’s coexisting chronic bronchitis is common

End-inspiratory crepitations and clubbing in asbestosis.

Signs of a pleural effusion or right heart failure (cor pulmonale).

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8
Q

Ix for pneumoconiosis

A

CXR

  • Simple – modular mottling
  • Complicated
    • Nodular opacities in the upper lobes
    • Micronodular shadowing
    • Diffuse military or nodular pattern in upper and mid-zones Eggshell calcification of hilar lymph nodes in silicosis
    • In asbestosis – bilateral lower zone reticulonodilar shadowing and pleural plaques, visible as white lines when calcified - most obvious on the diaphragmatic pleura or as ‘hollyleaf’ patterns.
  • Progressive massive fibrosis
    • Bilateral, upper-mid zone fibrotic masses (1-10cm)
    • Develop from periphery to hilum

CT

  • Fibrotic changes can be seen early

Bronchoscopy

  • Visualise changes
  • Allows for bronchalveolar lavage

Lung function test

  • Restrictive ventilatory defect, impaired gas function
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