Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pulm > Lec 17 Occupational Lung Disease > Flashcards

Lec 17 Occupational Lung Disease Flashcards

1
Q

What is mech of aerosol deposition in pneumoconiosis?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where do largest diameter particles deposit vs smaller?

A 
large = deposit in nasopharynx
smaller = go to alveoli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How are deposited particles cleared?

A

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

by alveolar macrophages –>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is silicosis?

A

exposure to silica; usually component of rock or sand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Who is at risk for silicosis?

A

sandblasters, rock miners, quarry workers, stonecutters

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is pathogenesis of silicosis?

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a silicotic nodule?

A
  • ongoing inflammatory process causes scarring and get acellular nodules
    at first small/discrete then become larger and coalesce
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is simple silicosis?

A

initially radiographic appearance = small, rounded nodules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is complicated silicosis?

A

nodules larger and coalesce

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are clinical feat of silicosis?

A
  • upper lung zones affected more heavily than lower lung zones
  • may have enlarged hilar lymph nodes
  • dyspnea is predominant symptom
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

mycobacteria infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is coal workers pneumoconiosis?

A

black lung = exposure to coal dust

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is pathogenesis of coal workers pneumoconiosis?

A
  • lots of dust inhaled and engulfed by macrophages –> macrophages go into interstitium and aggregate around respiratory bronchioles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is simple coal workers pneumoconiosis vs complicated?

A 
simple = have coal macules and nodules
complicated = bulky, irregular well-defined rubbery black tissue masses; more common in upper lobes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a coal macule?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a coal nodule?

A

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

from expsorue to coal dust admixed with silica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are clinical feat of simple CWP?

A

few symptoms if any

pulmonary function preserved

18
Q

What are clinical feat of complicated CWP?

A

pronounced symptoms

coalescent opacities; may cavitate or calcify

19
Q

What do you see in asbestos

A

pulmonary parenchymal fibrosis

20
Q

Who is at risk for asbestosis?

A

insulation, shipyward and construction workers

people who work with brake linings

21
Q

What types of lung disease can you get with asbestos?

A

asbestosis = pulm parenchyma fibrosis

pleural disease = plaques, fibrosis, mesothelioma

lung cancer

22
Q

What is pathogenesis of asbestosis?

A
  • 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
Q

What is pathology of asbestosis?

A

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

represents asbestos fibers coated by macrophages with iron-protein complex

24
Q

Which part of lungs most heavily involved in asbestosis?

A

lung bases, subpleural regions

25
Q

Where do earliest microscopic lesions appear in asbestosis?

A

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

26
Q

What do you see on radiology in asbestosis?

A

linear streaking most prominent at lung bases

when advanced may have honeycombing

often pleura thickening, localized plaques = evidence of pleural involvement

27
Q

What are asbestos pleural plaques?

A

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
Q

Who is at risk for berylliosis?

A

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

29
Q

What happens in berylliosis?

A
  • formation of non-necrotizing granulomas like in sarcoidosis; in lungs and hilar and mediastinal lymph
  • due to delayed hypersensitivity response to beryllium
30
Q

What test do you use to check for beryllium exposure?

A

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

31
Q

What is hypersensitivity pneumonitis?

A

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
Q

What are symptoms of hypersensitivity pneumonitis?

A

dyspnea, cough, chest tightness, headache

33
Q

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

A 
exposure = moldy hay
antigen = thermophilic actinomycetes
34
Q

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

A 
exposure = pigeons, parakeets
antigen = droppings, feathers, serum proteins
35
Q

What do IgG precipitating antibodies indicate about hypersensitivity pneumonitis?

A

indicate expsorue to antigen
do not indicate disease = just a marker

also not sensitive b/c serum precipitins may disapper over time

36
Q

What is classic triad of hypersensitivity pneumonitis pathology?

A
  • cellular bronchiolitis
  • interstitial mononuclear cell infiltrates
  • scattered small non-necrotizing granulomas
37
Q

What are clinical feat of acute hypersensitivity pneumonitis?

A
  • 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
Q

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

A

acute = fine little dots; ground glass appearance

chronic = honeycombing; traction bronchiectasis

39
Q

What are clinical feat of chronic hypersensitivity pneumonitis?

A
  • gradual dyspnea and couhg
  • fatigue, loss of appetite weight loss

exam –> tachypnea, rales, clubbing, restrictive or obstructive or combined PFTs

behaves like ILDs

40
Q

What is treatment for hypersensitivity pneumonitis?

A

avoid antigens

corticosteroids

Pulm (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions