Lec 17 Occupational Lung Disease

Question 1

What is mech of aerosol deposition in pneumoconiosis?

Answer 1

• 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

Question 2

Where do largest diameter particles deposit vs smaller?

Answer 2

large = deposit in nasopharynx
smaller = go to alveoli

Question 3

How are deposited particles cleared?

Answer 3

by mucociliary system –> moves particles up airway to pharynx where coughed up or swallowed

by alveolar macrophages –>

Question 4

What is silicosis?

Answer 4

exposure to silica; usually component of rock or sand

Question 5

Who is at risk for silicosis?

Answer 5

sandblasters, rock miners, quarry workers, stonecutters

usually need > 20 yrs of exposure; for sandblasters shorter periods

Question 6

What is pathogenesis of silicosis?

Answer 6

• 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

Question 7

What is a silicotic nodule?

Answer 7

• ongoing inflammatory process causes scarring and get acellular nodules
  at first small/discrete then become larger and coalesce

Question 8

What is simple silicosis?

Answer 8

initially radiographic appearance = small, rounded nodules

Question 9

What is complicated silicosis?

Answer 9

nodules larger and coalesce

Question 10

What are clinical feat of silicosis?

Answer 10

• upper lung zones affected more heavily than lower lung zones
• may have enlarged hilar lymph nodes
• dyspnea is predominant symptom

Question 11

People with silicosis are particularly susceptible to what kind of infection?

Answer 11

mycobacteria infection

Question 12

What is coal workers pneumoconiosis?

Answer 12

black lung = exposure to coal dust

Question 13

What is pathogenesis of coal workers pneumoconiosis?

Answer 13

• lots of dust inhaled and engulfed by macrophages –> macrophages go into interstitium and aggregate around respiratory bronchioles

Question 14

What is simple coal workers pneumoconiosis vs complicated?

Answer 14

simple = have coal macules and nodules
complicated = bulky, irregular well-defined rubbery black tissue masses; more common in upper lobes

Question 15

What is a coal macule?

Answer 15

aggregation of dust + dust laden macrophages around resp bronchioles surrounded by little tissue reaction

Question 16

What is a coal nodule?

Answer 16

consists of dusta nd dust laden macrphages and dense irregular depositions of collagen

from expsorue to coal dust admixed with silica

Question 17

What are clinical feat of simple CWP?

Answer 17

few symptoms if any

pulmonary function preserved

Question 18

What are clinical feat of complicated CWP?

Answer 18

pronounced symptoms

coalescent opacities; may cavitate or calcify

Question 19

What do you see in asbestos

Answer 19

pulmonary parenchymal fibrosis

Question 20

Who is at risk for asbestosis?

Answer 20

insulation, shipyward and construction workers

people who work with brake linings

Question 21

What types of lung disease can you get with asbestos?

Answer 21

asbestosis = pulm parenchyma fibrosis

pleural disease = plaques, fibrosis, mesothelioma

lung cancer

Question 22

What is pathogenesis of asbestosis?

Answer 22

• 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

Question 23

What is pathology of asbestosis?

Answer 23

characteristic ferruginous body = rod shaped wtih club ends yellow-brown in stained tissue

represents asbestos fibers coated by macrophages with iron-protein complex

Question 24

Which part of lungs most heavily involved in asbestosis?

Answer 24

lung bases, subpleural regions

Question 25

Where do earliest microscopic lesions appear in asbestosis?

Answer 25

appear around respiratory bronchioles w/ alveolitis that progresses to peribronchiolar fibrosis

Question 26

What do you see on radiology in asbestosis?

Answer 26

linear streaking most prominent at lung bases when advanced may have honeycombing often pleura thickening, localized plaques = evidence of pleural involvement

Question 27

What are asbestos pleural plaques?

Answer 27

distinct smooth white rased irregular lesions on parietal pleura avascular, acellular collagen in parallel do not cause symptoms = manifestation of asbestos exposure not disease

Question 28

Who is at risk for berylliosis?

Answer 28

people who make fluorescent light bulbs, work in aerospace, nuclear weapons, electronics

Question 29

What happens in berylliosis?

Answer 29

- formation of non-necrotizing granulomas like in sarcoidosis; in lungs and hilar and mediastinal lymph - due to delayed hypersensitivity response to beryllium

Question 30

What test do you use to check for beryllium exposure?

Answer 30

beryllium lymphocyte transformation test --> lymphocytes from pts with exposure proliferate when exposed to berylium salts in vitro

Question 31

What is hypersensitivity pneumonitis?

Answer 31

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

Question 32

What are symptoms of hypersensitivity pneumonitis?

Answer 32

dyspnea, cough, chest tightness, headache

Question 33

What is farmer's lung source of exposure? antigen?

Answer 33

``` exposure = moldy hay antigen = thermophilic actinomycetes ```

Question 34

What is bird breeder's lung source of exposure? antigen?

Answer 34

``` exposure = pigeons, parakeets antigen = droppings, feathers, serum proteins ```

Question 35

What do IgG precipitating antibodies indicate about hypersensitivity pneumonitis?

Answer 35

indicate expsorue to antigen do not indicate disease = just a marker also not sensitive b/c serum precipitins may disapper over time

Question 36

What is classic triad of hypersensitivity pneumonitis pathology?

Answer 36

- cellular bronchiolitis - interstitial mononuclear cell infiltrates - scattered small non-necrotizing granulomas

Question 37

What are clinical feat of acute hypersensitivity pneumonitis?

Answer 37

- 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

Question 38

What do you see on image in acute vs chronic hypersensitivity pneumonitis?

Answer 38

acute = fine little dots; ground glass appearance chronic = honeycombing; traction bronchiectasis

Question 39

What are clinical feat of chronic hypersensitivity pneumonitis?

Answer 39

- gradual dyspnea and couhg - fatigue, loss of appetite weight loss exam --> tachypnea, rales, clubbing, restrictive or obstructive or combined PFTs behaves like ILDs

Question 40

What is treatment for hypersensitivity pneumonitis?

Answer 40

avoid antigens | corticosteroids