Lec 17 Occupational Lung Disease Flashcards
What is mech of aerosol deposition in pneumoconiosis?
- impaction -> largest inspired particles fail to turn corners of respiratory tract
- sedimentation –> particles settle b/c of weight esp. in small airways
- diffusion –> random movement of particles due to continuous bombardment by gas molec
Where do largest diameter particles deposit vs smaller?
large = deposit in nasopharynx smaller = go to alveoli
How are deposited particles cleared?
by mucociliary system –> moves particles up airway to pharynx where coughed up or swallowed
by alveolar macrophages –>
What is silicosis?
exposure to silica; usually component of rock or sand
Who is at risk for silicosis?
sandblasters, rock miners, quarry workers, stonecutters
usually need > 20 yrs of exposure; for sandblasters shorter periods
What is pathogenesis of silicosis?
- silica particles in resp tract phagocytosed by alveolar macrophages –> release inflammatory TNF-alpha, IL-1, arachidonic acid
phagocytosis of silica particles leads to apoptotic cell death –> toxic silica particles released and reingested by other macrophages
eventually leads to fibrosis; initially localized around resp bronchioles then becomes more diffuse
What is a silicotic nodule?
- ongoing inflammatory process causes scarring and get acellular nodules
at first small/discrete then become larger and coalesce
What is simple silicosis?
initially radiographic appearance = small, rounded nodules
What is complicated silicosis?
nodules larger and coalesce
What are clinical feat of silicosis?
- upper lung zones affected more heavily than lower lung zones
- may have enlarged hilar lymph nodes
- dyspnea is predominant symptom
People with silicosis are particularly susceptible to what kind of infection?
mycobacteria infection
What is coal workers pneumoconiosis?
black lung = exposure to coal dust
What is pathogenesis of coal workers pneumoconiosis?
- lots of dust inhaled and engulfed by macrophages –> macrophages go into interstitium and aggregate around respiratory bronchioles
What is simple coal workers pneumoconiosis vs complicated?
simple = have coal macules and nodules complicated = bulky, irregular well-defined rubbery black tissue masses; more common in upper lobes
What is a coal macule?
aggregation of dust + dust laden macrophages around resp bronchioles surrounded by little tissue reaction
What is a coal nodule?
consists of dusta nd dust laden macrphages and dense irregular depositions of collagen
from expsorue to coal dust admixed with silica
What are clinical feat of simple CWP?
few symptoms if any
pulmonary function preserved
What are clinical feat of complicated CWP?
pronounced symptoms
coalescent opacities; may cavitate or calcify
What do you see in asbestos
pulmonary parenchymal fibrosis
Who is at risk for asbestosis?
insulation, shipyward and construction workers
people who work with brake linings
What types of lung disease can you get with asbestos?
asbestosis = pulm parenchyma fibrosis
pleural disease = plaques, fibrosis, mesothelioma
lung cancer
What is pathogenesis of asbestosis?
- small fibers phagocytosis and drained via lymphatics to pleural space
- longer fibers incompletely phagocytosed –> become core of asbestos body
- if dust load is high –> proinflammatory and cytotoxic agents released –> fibroblast recruitment and proliferation –> fibrosis
What is pathology of asbestosis?
characteristic ferruginous body = rod shaped wtih club ends yellow-brown in stained tissue
represents asbestos fibers coated by macrophages with iron-protein complex
Which part of lungs most heavily involved in asbestosis?
lung bases, subpleural regions
Where do earliest microscopic lesions appear in asbestosis?
appear around respiratory bronchioles w/ alveolitis that progresses to peribronchiolar fibrosis
What do you see on radiology in asbestosis?
linear streaking most prominent at lung bases
when advanced may have honeycombing
often pleura thickening, localized plaques = evidence of pleural involvement
What are asbestos pleural plaques?
distinct smooth white rased irregular lesions on parietal pleura
avascular, acellular collagen in parallel
do not cause symptoms = manifestation of asbestos exposure not disease
Who is at risk for berylliosis?
people who make fluorescent light bulbs, work in aerospace, nuclear weapons, electronics
What happens in berylliosis?
- formation of non-necrotizing granulomas like in sarcoidosis; in lungs and hilar and mediastinal lymph
- due to delayed hypersensitivity response to beryllium
What test do you use to check for beryllium exposure?
beryllium lymphocyte transformation test –> lymphocytes from pts with exposure proliferate when exposed to berylium salts in vitro
What is hypersensitivity pneumonitis?
mixed type III/IV hypersensitivity rxn to environmental antigen
due to repeated antigen exposure; immunologic sensitization of host to antigen + immune-mediated damage to lung
What are symptoms of hypersensitivity pneumonitis?
dyspnea, cough, chest tightness, headache
What is farmer’s lung source of exposure? antigen?
exposure = moldy hay antigen = thermophilic actinomycetes
What is bird breeder’s lung source of exposure? antigen?
exposure = pigeons, parakeets antigen = droppings, feathers, serum proteins
What do IgG precipitating antibodies indicate about hypersensitivity pneumonitis?
indicate expsorue to antigen
do not indicate disease = just a marker
also not sensitive b/c serum precipitins may disapper over time
What is classic triad of hypersensitivity pneumonitis pathology?
- cellular bronchiolitis
- interstitial mononuclear cell infiltrates
- scattered small non-necrotizing granulomas
What are clinical feat of acute hypersensitivity pneumonitis?
- begins 4-12 hrs after exposure w/ onset viral-like symptoms –> cough, dyspnea, chest tightness, fever, chill, headahce
- on exam –> tachypnea, rales, restrictive PFTs
- remove exposure to antigen –> symptoms subside in days
What do you see on image in acute vs chronic hypersensitivity pneumonitis?
acute = fine little dots; ground glass appearance
chronic = honeycombing; traction bronchiectasis
What are clinical feat of chronic hypersensitivity pneumonitis?
- gradual dyspnea and couhg
- fatigue, loss of appetite weight loss
exam –> tachypnea, rales, clubbing, restrictive or obstructive or combined PFTs
behaves like ILDs
What is treatment for hypersensitivity pneumonitis?
avoid antigens
corticosteroids
