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Flashcards in occupational lung disease Deck (28):
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1. Know the major determinants of site and severity of lung disease

1. Dose= duration x concentration. 2. Solubility= More water-soluble agents deposit in the upper airway (i.e. chlorine - nasopharyngeal mucosa); less water-soluble agents affect the distal airways/bronchioles (i.e. nitrogen oxides). 3. Particle size= Particles > 10 microns are filtered in the upper airway, particles <2.5 microns may affect the small airways and alveoli.

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2. Know the questions used in evaluation of occupational lung disease

History: Where do you work? What is your job title? What are your job duties? What are you exposed to?

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Physical exam findings in evaluation of occupational lung disease

usually non specific

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Diagnostic tests used in evaluation of occupational lung disease

Pulmonary function testing (PFTs), cardio-pulmonary exercise tolerance test, bronchial challenge testing, chest imaging (chest x-ray, high resolution chest CT), blood tests (eg, BeLPT or tests for antigen-specific antibodies), occasionally lung biopsy

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3. Know the 2 major categories of occupational/environmental lung diseases

Airway diseases and interstitial lung diseases

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4. Know the types of airways diseases and examples

occupational asthma, reactive airways dysfunction syndrome (RADS) aka irritant asthma, chronic obstructive pulmonary disease (COPD) from coal mine dust, constrictive/obliterative bronchiolitis

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5. Know the types of interstitial lung diseases and examples

 Pneumoconioses: asbestos-related lung diseases (asbestosis), silicosis, coal worker’s pneumoconiosis. Others: hypersensitivity pneumonitis, chronic beryllium disease

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•HMW compounds: animal proteins, baking flours and enzymes that trigger a specific IgE immunologic reaction.LMW compounds: isocyanates (spray paint/auto-body

PFTs show obstruction (low FEV1) and/or air trapping (increased RV) and/or decreased DLCO. Imaging : may be normal or show airway wall thickening, air trapping, emphysema

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Interstitial disease PFTs and imaging

•Pulmonary function testing: shows restriction (low TLC/FVC), decreased DLCO. Imaging: inflammation (centrilobular nodules, groundglass opacities) or fibrosis (rounded or linear opacities)

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Occupational asthma causes and mechanisms

•HMW compounds: animal proteins, baking flours and enzymes that trigger a specific IgE immunologic reaction. LMW compounds: isocyanates (spray paint/auto-bodyrepair), plicatic acid (western red cedar), epoxy resins, platinum compounds that may combine with endogenous proteins to create new antigenic determinants

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Occupational asthma presentation

Months to years after initial exposure. May have a temporal pattern such as getting better on weekends. Variable airflow obstruction, airway hyperresponsiveness, and airway inflammation

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Reactive airway dysfunction syndrome presentation

•NO LATENCY, symptom onset within 24-48 hours of exposure. Airway epithelial injury leads to persistent hyperresponsiveness and airflow obstruction

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Reactive airway dysfunction syndrome causes and mechanism

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

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Occupational COPD presentation

•cough, sputum, wheezing, chest tightness and dyspnea

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Occupational COPD causes and mechanism

•Causes: exposure to biomass combustion, respirable silica and coal mine dusts (mining), vanadium, organic dusts. Mechanism: oxidant injury, imbalance of proteases and anti-proteases

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Constrictive/Obliterative Bronchiolitis presentation

•subtle onset with cough, dyspnea, chest tightness. Pathologic injury of small airways causes extrinsic or intrinsic bronchiolar narrowing

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Constrictive/Obliterative Bronchiolitis causes

•exposure to noxious gases such as oxides of nitrogen and sulfur, dusts (combustion products), and chemicals (i.e. diacetyl flavoring in buttered popcorn – think flavor workers lung disease)

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Constrictive/Obliterative Bronchiolitis mechanism

Injury to bronchiolar epithelium results in excessive proliferation of granulation tissue, leading to narrowing or obliteration of the airway; submucosal or peribronchiolar fibrosis may lead to extrinsic narrowing or obliteration of bronchiolar lumen

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Asbestos lung disease cause and mechanism

•Cause: asbestos fibers – group of naturally-occurring hydrated magnesium silicates that when crushed, break into fibers (friable) Mechanism: direct toxic effects of fibers on pulmonary parenchymal cells, with release of various mediators by inflammatory cells

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Asbestos related lung diseases

Malignant: lung cancer and mesothelioma. Non malignant: benign asbestos pleural effusion, pleural thickening/calcifications/plaques, rounded atelectasis, and asbestosis (fibrosis usually affecting lower lung zones)

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Silicosis presentation

usually long latency, includes SOB and cough. Causes interstitial lung disease which can progress to fibrotic lung disease

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Silicosis causes and mechanism

•Causes: crystalline silica, exposed workers such as gold miners, foundry workers, sandblasters (stone-washed jean manufacturers. Mechanism: : generation of oxygen radicals that injure target pulmonary cells such as alveolar macrophages, leads to generation of inflammatory cytokines

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Coal Workers Pneumoconiosis presentation

usually cough, shortness of breath; pulmonary function testing may be normal, chest imaging typically demonstrates upper lobe small rounded nodular opacities; pathology may be notable for “dust macules".

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Coal Workers Pneumoconiosis causes and mechanism

Causes: inhalation of coal mine dust. Mechanism: generation of oxygen radicals that injure target pulmonary cells such as alveolar macrophages, leads to generation of inflammatory cytokines

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Chronic Beryllium Disease presentation

Subtle cough, dyspnea, chest tightness. Indistinguishable from sarcoidosis excepft for exposures

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Chronic Beryllium Disease causes and mechanism

Causes: beryllium (lightweight, strong metal used in aerospace engineering, nuclear bomb manufacturing, nuclear reactors, etc.). Mechanism: immune response to beryllium, often leading to granulomatous lung inflammation; some workers have a genetic susceptibility to beryllium’s effects, but there is also a dose-response relationship

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Hypersensitivity Pneumonitis presentation

acute symptoms – flu-like illness with respiratory symptoms; subacute/chronic HP – insidious onset. Immune response to animal proteins

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Hypersensitivity Pneumonitis cause and mechanism

Causes: some animal proteins (mainly birds), 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. Mechanism: T cell response