Lec 17 Occupational Lung Disease Flashcards Preview

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Flashcards in Lec 17 Occupational Lung Disease Deck (40):
1

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

2

Where do largest diameter particles deposit vs smaller?

large = deposit in nasopharynx
smaller = go to alveoli

3

How are deposited particles cleared?

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

by alveolar macrophages -->

4

What is silicosis?

exposure to silica; usually component of rock or sand

5

Who is at risk for silicosis?

sandblasters, rock miners, quarry workers, stonecutters

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

6

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

7

What is a silicotic nodule?

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

8

What is simple silicosis?

initially radiographic appearance = small, rounded nodules

9

What is complicated silicosis?

nodules larger and coalesce

10

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

11

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

mycobacteria infection

12

What is coal workers pneumoconiosis?

black lung = exposure to coal dust

13

What is pathogenesis of coal workers pneumoconiosis?

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

14

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

15

What is a coal macule?

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

16

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

17

What are clinical feat of simple CWP?

few symptoms if any
pulmonary function preserved

18

What are clinical feat of complicated CWP?

pronounced symptoms
coalescent opacities; may cavitate or calcify

19

What do you see in asbestos

pulmonary parenchymal fibrosis

20

Who is at risk for asbestosis?

insulation, shipyward and construction workers

people who work with brake linings

21

What types of lung disease can you get with asbestos?

asbestosis = pulm parenchyma fibrosis

pleural disease = plaques, fibrosis, mesothelioma

lung cancer

22

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

23

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

24

Which part of lungs most heavily involved in asbestosis?

lung bases, subpleural regions

25

Where do earliest microscopic lesions appear in asbestosis?

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

26

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

27

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

28

Who is at risk for berylliosis?

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

29

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

30

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

31

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

32

What are symptoms of hypersensitivity pneumonitis?

dyspnea, cough, chest tightness, headache

33

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

exposure = moldy hay
antigen = thermophilic actinomycetes

34

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

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

35

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

36

What is classic triad of hypersensitivity pneumonitis pathology?

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

37

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

38

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

acute = fine little dots; ground glass appearance

chronic = honeycombing; traction bronchiectasis

39

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

40

What is treatment for hypersensitivity pneumonitis?

avoid antigens
corticosteroids