Occupational Lung Disease Flashcards
Three mechanisms of aerosol deposition
Impaction
Sedimentation
Diffusion
Impaction
Largest inspired particles fail to turn corners of respiratory tract. Almost all particles >20uM and >5UM filtered by nose
Sedimentation
Gradual settling of particles because of weight. Particularly important for medium sized particles. Larger particles removed by impaction and small particles settle slowly. Occurs extensively in small airways.
Diffusion
Random movement of particles as a result of continuous bombardment by gas molecules. Occurs with smallest particles. Chiefly takes place in small airways and alveoli where distances to the wall are least.
How are deposited particles cleared?
Mucociliary system
Alveolar macrophages
Does mucociliary system work in alveoli?
No, that is where alveolar macrophages do their thing. They phagocytose foreign particles and can migrate to small airways and load onto escalator, or leave lung via lymphatics.
Do alveolar macrophages ever deposit stuff at the walls of the respiratory bronchioles?
Yeah! When the dust burden is large or the dust particles are toxic.
Silicosis
Happens to sandblasters, rock miners, quarry workers, stone cutters. Development of disease usually requires 20 years of exposure. But heavy doses can cause it to happen earlier.
Pathogenesis of silicosis
Silica particles in lower respiratory tract are phagocytosed by alveolar macrophages. Freshly cut silica particles are more pathogenic than older particles. Macrophages become activated and release inflammatory mediators like TNF alpha, IL-1, arachidonic acid metabolites). This causes apoptosis of macrophages and ingestion of the toxic silica particles by other macrophages. This process repeats leading to huge inflammation and eventually fibrosis of alveoli.
Where is the inflammatory of silicosis initally localized?
Around respiratory bronchioles but then becomes more diffuse in parenchyma.
Silicotic nodule
The product of the ongoing inflammation from silicosis. Acellular nodules composed of connective tissue. They are small and discrete to begin but then become larger and may coalesce.
Clinical features of Silicosis
CXR notable for small rounded opacities or nodules. Progressive massive fibrosis during complicated silicosis. Calcified hilar lymph nodes. Dyspnea is predominant symptom and susceptible to infections with mycobacteria (probably due to impaired macrophage function)
Where in the lungs does silicosis occur?
In the upper lung zone.
Coal worker’s Pneumoconiosis
Black lung. Exposure to coal dust.
Pathogenesis of CWP
Massive amounts of dust inhaled an engulfed my macrophages. Macrophages pass into interstitium and aggregate around respiratory bronchioles. The bronchioles dilate causing FOCAL DUST EMPHYSEMA. This process is much less fibrogenic than silica.
Features of simple CWP
Coal macules and nodules
Coal macule
Aggregation of dust and dust laden macrophages around respiratory bronchioles surrounded by reslatively little tissue reaction
coal nodule consists of dust and dust laded macrhophages and esned irregular depositons of collagen result from exuposure to coald udst admixed with silica
Need!
Complicated coal workers pneumoconiosis
Fibrosis occurs basically. Happens in very few individuals.
Clinical features of simple CWP
Not many symptoms
Asbestos
See the rest of the lecture for this shit. Fuck. Just know that asbestos bodies exist and that the common site of involvement is the bottom of the lungs.
Pleural plaques
A major feature of asbestosis. These are collagen fibers arranged parallel to surface. Calcification common.
Berylliosis
Results from inhalation of metal dust from beryllium. Happens in people who make fluorescent light bulbs. Pathologic reaction found in lungs as well as hilar and mediastinal lymph nodes. Formation of granulomas that resemble sarcoidosis.
Beryllium lymphocyte transformation test
Lymphocytes harvested from people with berylliosis demonstrate transformation and proliferation when exposed to beryllium salts
Hypersensitivity pneumonitis
Result of immunologic phenomena directed against an antigen. Repeated antigen exposure and immunological sensitization of host to antigen. Immune mediated damage to the lung. Deposits into respiratory bronchioles. Can be acute, chronic, and subacute.
Two most common antigens of HP
Farmer’s lung (from moldy hay – thermophilic actinomyctes)
Bird Breeder’s Lung (from droppings, feathers, serum proteins of pidgeons and parakeets).
How to test for HP?
IgG precipitating antibodies . Indicates exposure not disease.
Classic HP pathological triad
Cellular bronchiolitis (airway-centered inflammation), interstitial mononuclear cell infiltrates, scattered small nonnectrotizing granulomas that are LOOSELY formed.
Acute HP features
4-12 hours after exposure. Viral-like respiratory illness. Cough dyspnea, fevers, chills, myalgias.
Demonstrates a restrictive ventilatory defect.
How to treat HP
Remove from antigen which causes symptoms to subside in like 12 hours. Also steroids.
Chronic HP
Insidious development of dyspnea and cough. PFTs are restrictive/obstructive/combined. This is particularly difficult.
