occupational lung disease Flashcards

1
Q

what information do you need to get when taking an occupational history?

A
  • type of mineral
  • duration
  • intensity
  • temporal relationship to onset symptoms
  • do symptoms improve when away from the workplace
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2
Q

what is pneumoconioses?

A
  • uncomplicated CWP: mild disease

- progressive massive fibrosis: activation of alveolar macrophages, progressive scarring causing stiff lungs

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3
Q

what happens with fibrotic lung disease?

A
  • activation of macrophages
  • restrictive lung function deficit
  • eggshell calcification of lymph nodes
  • risk factor for TB and lung cancer
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4
Q

how do you treat pneumoconioses?

A
  • prevent further exposure
  • stop smoking
  • monitor lung function
  • symptomatic treatment: cough, dyspnoea
  • no specific treatment or cure of disease itself
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5
Q

what benign issues does asbestos cause?

A
  • pleural plaques
  • benign pleural effusion
  • pleural thickening
  • asbestosis: interstitial lung disease-restrictive lung function with reduction in forced vital capacity and reduced gas transfer
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6
Q

what malignant issues does asbestos cause?

A
  • lung cancer
  • mesothelioma: malignancy of pleura and peritoneum caused by asbestos, consider patient history: pleural plaques on chest x-ray, persistent unexplained chest pain, weight loss, breathless/unilateral pleural effusion
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7
Q

what are the 2 distinct scenarios of occupational asthma (OA)?

A

1) occupational asthma caused by workplace exposures

2) work aggravated asthma in which pre-existing causes are made worse by factors in the workplace

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8
Q

what are the personal factors that need to be taken into account when diagnosis of occupational asthma (OA)?

A
  • is it really asthma?
  • consider OA in all patients presenting with asthma in adult life
  • failure to respond to asthma Rx
  • other risks factors: atopy, rhinitis, smoking
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9
Q

what are the workplace factors that need to be taken into account when diagnosis of occupational asthma (OA)?

A
  • recognition of high risk job
  • co-workers similarly affected
  • recent changed: products, tasks undertaken
  • preventative measures: ventilation, masks
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10
Q

what are the other factors that need to be taken into account when diagnosis of occupational asthma (OA)?

A
  • have they lost their job already?
  • are they seeking compensation?
  • establishing a casual link can be hard
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11
Q

what is the role of challenge testing?

A
  • confirm diagnosis when new agent blamed
  • identify responsible agent when multiple sensisters in workplace
  • confirm diagnosis when history and PEFR records are equivocal
  • rarely to exclude diagnosis in patient who will otherwise lose their job
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12
Q

what are the criteria to fit for challenge testing & what happens?

A
  • asthma should be stable
  • withhold bronchodilators
  • a placebo exposure day is advisable
  • equipment that delivers known concentration of suspected agent
  • monitor spirometry for several hours after each increase in exposure day
  • may take several days
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13
Q

what is irritant-induced/non-allergic asthma?

A

direct effect on airways, not immune mediated occurs without pre-existing asthma

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14
Q

what is acute irritant-induced/non-allergic asthma?

A

reactive airways dysfunction syndrome (RADS): develops within hours of a single, very high exposure

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15
Q

what is subacute irritant-induced/non-allergic asthma?

A

insidious onset of asthma symptoms after multiple moderate/high empire incidents

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16
Q

what are the causative agents of RADS?

A
  • caustic vapours
  • ammonia
  • fire/smoke
  • chorine
  • tear gas
  • floor sealants
17
Q

what is a toxin?

A

a naturally occurring poison produced within living cells or organism

18
Q

what is a pollutant?

A

any substance that contaminates the enviroments

19
Q

what is exposure a function of?

A
  • concentration of toxin/pollutants
  • duration
  • intensity
  • route
  • metabolism of toxin
  • clinical impact varies with an individual
20
Q

what increases susceptibility to occupational lung diseases?

A
  • genetic factors
  • co-morbidity/underlying diseases that augment clinical impact of toxic load
  • environmental factors: heat waves, cold snaps, smog
21
Q

what are primary pollutants?

A
  • from fossil fuel combustion
  • nitrogen oxide
  • sulphur dioxide
  • carbon monoxide
  • particulate matter
22
Q

what are secondary pollutants?

A

from reactions between pollutants in the atmosphere

23
Q

what happens with nitrogen oxides?

A
  • associated with COPD and asthma
  • augments response to inhaled allergens
  • increased likelihood that URTI will cause wheezing in children
24
Q

what are the health issues associated with ground-level ozone?

A
  • decreased lung function
  • pro-inflammatory effects
  • increased response to inhaled allergens
  • increased respiratory morbidity
25
Q

how does particulate matter affect airway structural elements?

A
  • airway cilia
  • mucous production
  • oxidating stress to cell DNA
  • infection of epithelial apoptosis
  • promoted airway inflammation and increased IgE production