M103 T4 L17 Flashcards

1
Q

What are the different types of occupational lung diseases?

A

COPD
Malignant diseases
Occupational asthma
Pneumoconioses (mineral dust)

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2
Q

What are examples of malignant occupational lung diseases?

A
Lung cancer (asbestos and non asbestos related)
Mesothelioma
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3
Q

What are examples of pneumoconioses? (CAS)

A

Coal Workers’ Lung
Asbestosis
Silicosis

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4
Q

What are pneumoconioses caused by?

A

the inhalation of certain dusts

the lung tissue’s reaction to the dust

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5
Q

Which job occupations are linked to silicosis?

A
Slate workers (Wales)
Potters (Stoke-on-Trent)
Knife grinders (Sheffield)
Hard rock miners (Canada etc)
Sand-blasting
Foundry workers
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6
Q

What is silicosis a risk factor for?

A

lung cancer

TB

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7
Q

What is the main aim for treatment of pneumoconioses?

A

to prevent further exposure

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8
Q

Which symptoms of pneumoconioses have to be managed? (BCCD)

A

breathlessness, cough, cor pulmonale & dyspnoea

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9
Q

Which areas was asbestos historically mined in?

A

Canada
Australia
South Africa

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10
Q

How did asbestos get to the UK?

A

it was imported via docks (esp Southampton)

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11
Q

When was asbestos widely used?

A

in the 1930s-70s

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12
Q

What was asbestos used in?

A
building (roofs, insulation, plumbing)
power stations
ship-building (engine rooms, bulkheads)
railways
cars (brake pads)
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13
Q

Other than from working in astestos-containing environments, how else could people get related illnesses?

A

family members at home who washed contaminated clothes

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14
Q

When did Europe bring in a ban on all forms of asbestos?

A

2005

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15
Q

Is asbestos still used?

A

yes, there are other countries outside of teh EU that are mining and exporting asbestos

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16
Q

Which benign conditions can asbestos cause?

A

pleural plaques / thickening
benign pleural effusion
asbestosis

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17
Q

What is the effect of pleural thickening?

A

restriction on lung function

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18
Q

What do pleural plaques indicate?

A

they are a marker of exposure

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19
Q

What pattern is seen on the lung function of a patient with penumoconioses?

A

a restrictive pattern of abnormality

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20
Q

How would FVC and gas transfer of a patient with pneumoconioses be affected?

A

FVC - reduced

gas transfer - reduced

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21
Q

Which malignant diseases can asbestos cause?

A

lung cancer

mesothelioma

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22
Q

What features of a patient history can indicate a malignant disease caused by asbestos?

A

Pleural plaques on previous CXRs
persistent unexplained chest pain
Weight loss
Breathless / unilateral pleural effusion

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23
Q

What are the two distinct scenarios of asthma related to work?

A

occupational

work-aggrevated

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24
Q

What is occupational asthma caused by?

A

by workplace exposure to asbestos

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25
What is work-aggrevated asthma caused by?
by pre-existing cases that are exacerbated by asbestos in the workplace
26
What are the other risk factors of occupational asthma? (SAR)
smoking atopy rhinitis
27
What are two types of features in substances might lead to allergic occupational asthma?
HMW (80-90% cases) | LMW
28
Which HMW substances can be assessed for by skin prick / allergy testing? (FALE)
Flour (bakers) Animals (farmers) Latex Enzymes (eg detergents)
29
What is the relationship between LMW or HMW substances and IgE antibodies?
low - independent of IgE | high - IgE-dependent
30
Which LMW substances can be assessed for by skin prick / allergy testing in limited circumstances?
Isocyanates (printing, plastics) Metals (welders) Dyes (hairdressers)
31
What might be a consequence of irritant induced asthma?
the patient developing asthma
32
What are the two types of irritant induced asthma?
acute | subacute
33
What is an example of an acute irritant induced asthma?
Reactive Airways Dysfunction Syndrome
34
What substances can cause Reactive Airways Dysfunction Syndrome? Can Chlorine Arise From Teachers Failing
``` Caustic vapours Chlorine Ammonia Fire/Smoke Tear Gas Floor Sealants ```
35
What factors does exposure to a certain toxin depend on?
the concentration of the toxin / pollutant the duration and intensity of the exposure the route by which the exposure occured (skin vs inhaled) the mechanism and metabolism of the toxin any co-morbidities of the patient
36
Which factors determine a patient's susceptibility to developing allergic occupational asthma?
Genetic factors Co-morbidity / underlying diseases Environmental factors
37
Which Genetic factor might contribute to a patient developing allergic occupational asthma?
the protective effect of HbS against falciparum malaria
38
What are examples of Environmental factors that might contribute to a patient developing allergic occupational asthma?
Heat waves cold snaps smogs
39
Why might a co morbidity contribute to a patient developing allergic occupational asthma?
the co morbidity might augment the clinical impact of the toxic load
40
What is the difference between primary and secondary pollutants?
1o - are from fossil fuel combustion | 2o - are from reactions between pollutants in the atmosphere
41
What are examples of primary pollutants?
Nitrogen oxide Sulphur dioxide (diesel) Carbon monoxide Particulate matter
42
What are the outdoor sources of NO?
vehicle exhausts | power stations
43
What are the indoor sources of NO?
fuel burning cookers unfueled heaters cigarette smoke
44
What conditions are NOs associated with?
COPD | asthma
45
What are the health effects of ground level ozone?
decreases lung function decreases pro-inflammatory effects increases response to inhaled allergens increases respiratory morbidity
46
What structures in the airways are affected by particulate matter?
cilia cell DNA mucus epithelium
47
What is the effect of airway structural elements on the human body?
affects airway structural elements promotes airway inflammation promotes IgE production
48
What are the two categories of exposure that can be reduced?
Occupational | Environmental
49
What can be done to reduce Occupational exposure to pollutants?
the use of FFP3 masks | Ventilation / extraction of chemicals
50
What can be done to reduce Environmental exposure to pollutants?
Air quality warnings Remain indoors, close windows Minimise duration/intensity of outdoor activities
51
Why are airway provocation tests performed in the first place?
bc people with sensitive lungs will be affected by a much lower dose of this medication than people with healthy lungs
52
What is the objective of airway provocation tests?
to carefully to make sure specific drugs for individual patients is safe
53
How do airway provocation tests work?
by breathing in gradually increasing doses of a medication that can irritate the airways and cause them to get narrower
54
*g* What structures are indicative of Progressive Massive Fibrosis on CXRs?
a fibrotic pneumoconiotic lesion with a diameter of x > 1cm | the formation of large mass-like conglomerates, predominantly in the upper pulmonary lobes
55
*g* What are the consequences of Progressive Massive Fibrosis?
progressive scarring, causes stiff lungs
56
*g* What is Progressive Massive Fibrosis primarily caused by ?
conioses, which results in the activation of alveolar macrophages, which phagocytose dust particles after their deposition
57
What medication is used to manage a cough & breathlessness?
opiates
58
What medication is used to manage r. HF?
diuretics
59
What can specific IgE assays test for?
allergic reactions in most HMW allergens and some LMW agents
60
What are the effects of particulate matter in the airways?
Mucous production Oxidative stress to cell DNA Induction of epithelial apoptosis
61
What is the difference between FFP 1, FFP 2 or FFP 3 masks?
the higher the number, the better the protection against toxic substances