17: Occupational Lung Disease Flashcards

1
Q

**Occupational lung disease **definition

A
  • Group of illnesses caused by repeated, extended exposure to single or severe exposure to irritating or toxic substances thatleads to acute or chronic respiratory ailments.
    • Related to specific occupation
    • Aggravated at work
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2
Q

OLD pathogenesis

A
  • Asthma/bronchitis: immunologic or nonimmunologic airway hyperreactivity
  • Pneumoconioses: deposition > dust clearance; direct cytotoxicity; alveolar macrophage response –> granulomatous inflammation and fibrosis, cytokine recruitement
  • Hypersensitivity pneumonitis: allergic response to inhaled organic antigens
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3
Q

Particle size spectrum of OLD

A
  • 5-10um: asthma or bronchitis
  • 3-5um: bronchiolar dz
  • 0-3um: ILD
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4
Q

Occupational asthma

A
  • Variable airflow limitation and/or airway hyperresponsiveness due to stimuli in occupation environment (9-15% adult asthma)
  • Three types:
    • Immunologic: latency period (1-2yrs) –> immunological sensitization, IgE mediated, 90% of cases, Sx improve after work
    • Irritant-induced (nonimmunologic): exposure to ↑[irritants], damage to airway epithelium, 7% of cases, Sx w/in 24 hrs of exposure, no previous asthma Hx, not improved after work
    • Work-aggravated: pre-existing asthma
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5
Q

Silicosis

A
  • Occupations that disturb earth’s crust, use silica-containing rock/sand
  • Dx: Hx of exposure to silica (quartz, cristobalite, tridymite), abnormal CXR, exclusion of other etiologies
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6
Q

Acute silicosis

A
  • Exposure: weeks to 5 yrs
  • Post-exposure onset: 1-3 yrs
  • Sx: cough, constitutional Sx, dyspnea
  • Radiology: basilar alveolar filling process
  • Pathology: alveolar filling w/ PAS + lipo-proteinaceous material, interstitial thickening
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7
Q

Accelerated silicosis

A
  • Exposure: years
  • Post-exposure onset: < 10 yrs
  • Sx: same as acute + arthralgia
  • PFTs: mixed obstructive-restrictive deficit
  • Radiology: 2-6mm nodules, upper & posterior location, hilar LAN, +/- eggshell calcification
  • Pathology: silicotic nodules (hyalinized center, concentrically arranged collagen, weakly birefringent particles, macrophages & lymphocytes at outer rim)
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8
Q

Chronic silicosis

A
  • Exposure: decades
  • Post-exposure onset: 10-30yrs
  • Sx: None, chronic cough, dyspnea
  • PFTs: mixed obstructive-restrictive deficit
  • Radiology & pathology same as accelerated silicosis
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9
Q

Progressive massive fibrosis (PMF)

A
  • Severest form of silicosis
  • Exposure: decades
  • Post-exposure onset: 10-30 yrs
  • Sx: progressive dyspnea +/- cor pulmonale
  • Mixed obstructive-restrictive deficit
  • Radiology: coalescing nodules (>1cm) +/- central necrosis, hilar retraction upward, hyperinflation lower lung zones
  • Pathology: coalescence of silicotic nodules
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10
Q

Silicosis complications

A
  • Mycobacterial dz: 2.8x > RR of TB
  • Immune-mediated: ↑auto-Ab, ↑auto-immune dz
  • Bronchitis/airflow obstruction
  • Lung cancer
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11
Q

Silicosis treatment

A
  • Corticosteroids
  • Whole lung lavage
  • Transplantation
  • Prevention (respirator mask)
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12
Q

Asbestos-related lung disease

A
  • Parenchymal: asbestosis
  • Pleural: pleural plaques, BAPE & pleural thickening, atelectasis
  • Malignancy: lung cancer, mesothelioma
  • 15-35 yr latency from exposure
  • Ongoing sites of major production:
    • Amphobile: South Africa, Australia
    • Chrysostile: Russia, China
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13
Q

**Asbestosis **mechanism

A
  • Exposure
  • Injury: cell apoptosis, mitochondrial ROS production and DNA damage, macrophage phagocytosis, H2O2 production, cytokine release
  • Fibrosis: myofibroblast proliferation
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14
Q

Asbestosis diagnosis

A
  • Hx of asbestos exposure
  • Bilateral pleural plaques
  • BAL fluid or Bx w/ increased [asbestos fibers] or [asbestos bodies] –> ferruginous bodies
  • Characteristic HRCT findings
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15
Q

Asbestosis

A
  • Clinical: cough, dyspnea, diffuse interstitial fibrosis, restrictive PFTs
  • Radiology: HRCT has lower lobe, subpleural, linear interstitial markings, parenchymal bands, intra/interlobular septal thickening, honeycomb change, pleural plaques
  • Pathology: ↑asbestos bodies, UIP pattern
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16
Q

Pleural disease from asbestos

A
  • Pleural plaques, pleural adhesions, Benign Asbestos Pleural Effusion (BAPE)
  • Clinical: asymptomatic
  • Radiology: parietal plaques 6-9th ribs & diaphragm, sparing of CPAs & apices, rounded atelectasis (“comet tails”), unilateral +/- advance pleural thickening
  • Pathology: acellular w/ collagen bundles, pleural inflammation & fibrosis, exudate
17
Q

Asbestos & malignancy

A
  • Primary lung cancer:
    • 6x > RR if non-smoker
    • 59x > RR if smoker
  • Malignant mesothelioma