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CVPR: Pulmonary > Occupational Lung Disease > Flashcards

Occupational Lung Disease Flashcards

1
Q

Major airway diseases related to occupational exposure

A
  • occupational asthma
  • reactive airways dysfxn syndrome (RADS)
  • COPD
  • constrictive/obliterative bronchiolitis
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2
Q

Major interstitial lung diseases related to occupational exposure

A
  • asbestos-related lung diseases (asbestosis),
  • silicosis
  • coal worker’s pneumoconiosis
  • hypersensitivity pneumonitis
  • chronic beryllium disease
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3
Q

Major Hx questions to determine presence of occupational lung disease

A
  • Where do you work?
  • What is your job title?
  • What are your job duties?
  • What are you exposed to?
  • Review exposure assessment: MSDS, OSHA reports, exposure sampling
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4
Q

Major determinants of site/severity of lung disease

A
  • dose: duration*concentration
  • solubility
  • particle size
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5
Q

Impact of solubility on site/severity of lung disease

A
  • more water-soluble agents ==> upper airway (i.e. nasopharyngeal mucosa, eg, chlorine)
  • less water-soluble agents ==> distal airways/bronchioles (eg, nitrogen oxides).
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6
Q

Impact of particle size on site/severity of lung disease

A
  • particles > 10 microns = upper airway
  • particles <10 microns are “respirable” = more deeply into the lung
  • particles <2.5 microns = small airways and alveoli
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7
Q

Occupational asthma (OA) general characteristics

A
  • airway dz w/variable otuflow obstruction + airway hyperresponse + airway inflammation due to occupational exposure
  • caused by agents w/immunologic/sensitizing properties
  • OA and asbestos-related lung disease = most common occupational lung diseases
  • OA accounts for up to 15% of adult asthma.
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8
Q

OA: causes/mechanisms

A

i. High-molecular weight compounds – eg, animal proteins, baking flours and enzymes that trigger a specific IgE immunologic reaction
ii. Low-molecular weight compounds – eg, isocyanates, plicatic acid (found in western red cedar), epoxy resins, platinum compounds <== combine w/self proteins to create new “foreign” antigens

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9
Q

OA: Dx & Tx

A
  • asthma w/latency = onset long after exposure
    • usually improves w/time away from work
  • confirm asthma w/PFTs and imaging
  • Tx: remove causal exposure + normal asthma tx
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10
Q

RADS general characteristics

A

Airway epithelial injury from exposure to inhalants with irritant properties, leading to persistent bronchial hyperresponsiveness and airflow obstruction

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11
Q

RADS: causes & mechanism

A

i. Causes: exposure to noxious irritant gas/vapor/dusts (eg, World Trade Center workers exposed to high pH alkaline dust)
ii. Mechanism: denudation of the mucosa with fibrinohemorrhagic exudates in the submucosa, followed by proliferation of basal cells and subepithelial edema. May expose airway c-fibers, triggering cough and bronchospasm.

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12
Q

RADS: Dx & Tx

A
  • No latency = sx w/in 24-48 hrs of expsure
  • Dx w/Hx, PFTs, imaging
  • Tx w/asthma Rx
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13
Q

COPD (occupational): Causes & Mechanism

A

i. 15% of COPD due to occupational causes including biomass combustion, respirable silica and coal mine dusts (mining), organic dusts
ii. Mechanism: probably similar to tobacco-smoke induced COPD – oxidant injury, imbalance of proteases and anti-proteases

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14
Q

COPD: Dx & Tx

A
  • Sx: cough, sputum, wheezing, chest tightness, dyspnea
  • Dx w/PFTs, imaging, hx
  • Tx: remove from exposure, COPD rx
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15
Q

Constrictive/Obliterative Bronchiolitis: definition

A

Pathologic injury of small airways (eg, less than 2 mm in diameter), with extrinsic or intrinsic bronchiolar narrowing

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16
Q

Constrictive/Obliterative Bronchiolitis: causes & mechanism

A

i. Causes: Exposure to some noxious gases (eg, oxides of nitrogen and sulfur), dusts (combustion products), and chemicals (eg, diacetyl flavoring in buttered popcorn)
ii. Mechanism: a. Injury to the bronchiolar epithelium ==> granulation tissue ==> narrowing or obliteration of the airway.
b. Submucosal or peribronchiolar fibrosis ==> extrinsic narrowing or obliteration of the bronchiolar lumen.

17
Q

Constrictive/Obliterative Bronchiolitis: Dx & Tx

A
  • sx: subtle onset, cough, dyspnea, chest tight
  • dx: hx, PFTs, CT shows air trapping
  • tx: remove from exposure (poor prognosis)
18
Q

Asbestos-related Lung diseases: causes & mechanism

A
  • asbestos = metallic fiber ==> shape/size (aspect ratio) confer disease risk
  • main exposures: construction demolition/remodels, commercial brake mechanics
  • Direct toxic effects of fibers on pulmonary parenchymal cells
    • Free radicals react with and damage a variety of cellular macromolecules and may disrupt DNA, increasing risk for malignancy.
19
Q

Types of non-malignant asbestos-related lung disease

A
  • benign asbestos pleural effusion
  • pleural thickening/calcification/plaque
  • rounded atelectasis
  • asbestosis
20
Q

Types of malignant asbestos-related lung disease

A
  • lung cancer <== syngery with smoking (asbestos + smoking = 50x increased risk)
  • mesothelioma (pleural, peritoneal)
    • no increased risk w/ smoking
    • sentinel cancer for asbestos exposure
21
Q

Asbestos-related lung diseases: Dx & Tx

A
  • Hx (early occupations), PFTs (restricted), imaging (plaques, scarring)
  • Tx: benign=supportive, malignant=oncology; remove from exposure
22
Q

Silicosis: causes & mechanism

A
  • Workers who blast, cut, grind with/on respirable silica containing materials
    • Hard rock miners, foundry workers, sandblasters, stone-washed jeans manufacturers
  • ​O2 radicals injure target pulmonary cells such as alveolar macrophages ==> inflammatory cytokines ==> resulting in inflammation and fibrosis
23
Q

Silicosis: Types

A
  • simple silicosis
  • complicated silicosis (progressive massive fibrosis)
  • acute silicoproteinsosis
  • accelerated silicosis
  • other conditions can result (infections, cancer, etc.)
24
Q

Silicosis: Dx & Tx

A
  • Dx: exposure history, PFTs (restriced or mixed)
    • imaging: upper lobe, nodular, silicoprotein=~PNA-looking
    • biopsy
  • Tx: removal from exposure
25
Q

Workers pneumoconiosis (Black lung): causes, mechanism, dx, tx

A
  • Cause: inhalation of coal mine dust , underground > surface
  • Mechanism: similar to silica toxicity
  • Diagnosis: exposure hx, PFTs (normal or abormal), imaging (upper lobe small rounded nodular opacities)
    • Pathologic feature = “dust macule”
  • Treatment: remove exposure, pulmonary supportive care
26
Q

Chronic Beryllium disease (CBD): cause & mechanism

A
  • Beryllium (Be) = metal in aerospace/bomb manufacture ==> beryllium sensitization
  • Mechanism: Immune response to beryllium ==> granulomatous lung inflammation.
    • some genetic susceptibility possible
    • dose-response relationship
27
Q

Chronic Beryllium disease (CBD): Dx & Tx

A
  • Dx: hx of exposure, latency, dyspnea, cough
    • blood levels of BeLPT
    • lung biopsy
  • Tx: remove from exposure, inhaled steriods
28
Q

Hypersensitivity Pneumonitis: causes & mechanism

A

i. Causes :
1. Some animal proteins (mainly birds) – parrots, cockatiels, cockatoos, finches (Bird fancier’s lung)
2. Microbial aerosols: fungi, bacteria inhaled from contaminated hay (Farmer’s Lung), hot tubs & indoor pools (due to non-tuberculous mycobacteria and gram-negative organisms), humidifiers, machining/metal-working fluids
3. A few low molecular weight chemicals: isocyanates
ii. Mechanism
1. T-cell-mediated immune response, with antigen-specific antibodies

29
Q

Hypersenstivity Pneumonitis: Dx & Tx

A
  • Acute: flu-like, respiratory illness, 6-12 hrs after high-dose exposure
  • Subacute/Chornic: respiratory + systemic symptoms
  • Dx: exposure hx, PFTs (restricted usuallly), CT w/ upper lobe centrilobular nodes, ground glass, air trapping

CVPR: Pulmonary (35 decks)

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