Clin Med: Occupational Lung Disease Flashcards

1
Q

Coal workers pneumoconiosis is due to

A

carbon containing particulate from coal mining

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2
Q

Coal workers pneumoconiosis aka =

A

‘black lung’
anthracosis
anthrasilicosis

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3
Q

longer time in occupation =

A

higher risk

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4
Q

Coal workers pneumoconiosis presentation

A

primarily asymptomatic
if sx develop they are non-specific:
SOB exertion to rest
Cough
Sputum production +/- black tinge
Chest tightness

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5
Q

Coal workers pneumoconiosis workup

A

CXR - alveolar macrophages - coal macules, 2-5 diffuse, small, round, nodular opacities on CXR, upper lungs often with granular appearance
PFTs - CWP produces minimal PFT changes but can coexist with chronic bronchitis and/or COPD
+/- Chest CT - some lymph node enlargement

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6
Q

Coal workers pneumoconiosis treatment

A

no cure or definitive treatment
supportive:
bronchodilators, pulm rehab, suppl O2, smoking cessation, lung transplant

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7
Q

Coal workers pneumoconiosis complications

A

Pulm HTN
R-sided HF
Resp failure
Premature death

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8
Q

Coal workers pneumoconiosis treatment goal

A

identify CWP early through screening
CXR
Include PFTs

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9
Q

Screening protocol for CWP

A

baseline CXR then f/u at 3 years
Routine offered a min of once every 5 years
F/u screen every 2 years if any abnormal

screenings offered every year but at pts expense

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10
Q

Coal workers pneumoconiosis prevention

A

PPE
education on acceptable working conditions
avoid smoking or smoking cessation
encourage periodic screenings

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11
Q

Silicosis causative agent

A

silica dust

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12
Q

Silicosis main forms

A

Acute Silicosis from large volume exposure (high mortality)
Accelerated form from 5-10 years of exposure
Chronic form from 15-20 years of exposure

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13
Q

Silicosis acute presentation

A

dyspnea
wt loss
fatigue
diffuse bilateral crackles
respiratory failure within 2 years

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14
Q

Silicosis chronic/ accelerated presentation

A

primarily asymptomatic
sx non-specific:
SOB
cough
sputum production

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15
Q

Dx of Silicosis

A

Chest CT preferred - better to differentiate from asbestosis
CXR
PFTs

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16
Q

Findings on CT for Silicosis

A

1-3mm small round opacities mostly upper lung fields
mediastinal and hilar lymphadenopathy
+/- lymph node calcifications - eggshell calcifications

Acute Silicosis = bilateral consolidation with ground glass opacities

17
Q

Silicosis treatment

A

no cure or definitive treatment
supportive:
bronchodilators, inhaled corticosteroids, pulm rehab, lung transplant

18
Q

Silicosis complications

A

TB and non-tb mycobacterial infections**
Spontaneous pneumothorax
emphysema
lung cancer**
pulm HTN
resp failure

19
Q

Silicosis prevention

A

best treatment is prevention
industrial intervention
PPE
screenings
smoking cessation
pneumo and flu vaccines in at risk pts

20
Q

Asbestosis causative agent

A

asbestos (old home remodeling, heat, fire, chemically, electrical resistant material)
Direct toxic and macrophage activation -> inflammation -> fibrosis

21
Q

Asbestosis dose dependent =

A

10-15 years post exposure

22
Q

Asbestosis presentation

A

primarily asymptomatic
if sx they are non-specific:
SOB
non-productive cough **
fatigue
clubbing of digits - sign of hypoxia
bibasilar crackles

23
Q

Dx Asbestosis workup

A

CT chest preferred
CXR
lung bx to confirm (rarely necessary)
PFTs for monitoring of progression

24
Q

CT chest for Asbestosis shows

A

bilateral linear reticular opacities (honeycombing)
predilection of lower lungs
pleural plaques** (pathognomic)

25
Q

Treatment for Asbestosis

A

no cure or definitive treatment
symptomatic relief

26
Q

Asbestosis complications

A

lung cancer - mesothelioma (main cause if Asbestosis), non-small cell lung cancer (bigger risk but other things can cause as well)***
Pulmonary HTN
R-sided HF
Resp failure
premature death

27
Q

Asbestosis prevention

A

annual lung cancer screening (low dose CT scan)
smoking cessation
flu and pneumococcal immunizations

28
Q

Hypersensitivity Pneumonitis exposure to causative agent leads to

A

exposure to agent –> inflammation
aka extrinsic allergic alveolitis

29
Q

Hypersensitivity Pneumonitis primarily manifests as

A

acute illness 4-8 hours after exposure

30
Q

Symptoms of Hypersensitivity Pneumonitis

A

fever
chills
malaise
cough
dyspnea
nausea

31
Q

PE for Hypersensitivity Pneumonitis

A

bibasilar crackles
resp distress:
tachycardia
tachypnea
+/- cyanosis

32
Q

Hypersensitivity Pneumonitis workup

A

CXR - small nodular densities in the central lungs
CBC - elevated WBC count
check for antibodies to common substances
restrictive pattern on PFTs

33
Q

Hypersensitivity Pneumonitis treatment

A

oral corticosteroids if severe
avoid further exposure
likely occupational change

34
Q

Smoke inhalation 3 possible mechanisms of damage

A
  1. impaired Oxygenation – CO or cyanide - oxygen displacement
  2. upper airway thermal burns
  3. lower airway chemical injury or physical irritants
35
Q

sign of inhalation injury

A

occurred in enclosed space
singed nasal hair or burns on lips
deep or full thickness burns to face, neck, upper torso
black colored sputum or soot around nasal passages

36
Q

Smoking inhalation treatment

A

100% O2 to treat any CO poisoning
Humidification O2 or helium -O2 mixture too aid in breathing
Bronchodilators
monitor hypoxia
intubation
suctioning or chest PT
fluid resuscitation

37
Q

what can monitor infection from smoking inhalation daily

A

Sputum cultures
Prophylactic abx not indicated