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.
