Lec 17 Occupational Lung Disease Flashcards Preview

Pulm > Lec 17 Occupational Lung Disease > Flashcards

Flashcards in Lec 17 Occupational Lung Disease Deck (40):

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