Clin Med: Occupational Lung Disease Flashcards
Coal workers pneumoconiosis is due to
carbon containing particulate from coal mining
Coal workers pneumoconiosis aka =
‘black lung’
anthracosis
anthrasilicosis
longer time in occupation =
higher risk
Coal workers pneumoconiosis presentation
primarily asymptomatic
if sx develop they are non-specific:
SOB exertion to rest
Cough
Sputum production +/- black tinge
Chest tightness
Coal workers pneumoconiosis workup
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
Coal workers pneumoconiosis treatment
no cure or definitive treatment
supportive:
bronchodilators, pulm rehab, suppl O2, smoking cessation, lung transplant
Coal workers pneumoconiosis complications
Pulm HTN
R-sided HF
Resp failure
Premature death
Coal workers pneumoconiosis treatment goal
identify CWP early through screening
CXR
Include PFTs
Screening protocol for CWP
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
Coal workers pneumoconiosis prevention
PPE
education on acceptable working conditions
avoid smoking or smoking cessation
encourage periodic screenings
Silicosis causative agent
silica dust
Silicosis main forms
Acute Silicosis from large volume exposure (high mortality)
Accelerated form from 5-10 years of exposure
Chronic form from 15-20 years of exposure
Silicosis acute presentation
dyspnea
wt loss
fatigue
diffuse bilateral crackles
respiratory failure within 2 years
Silicosis chronic/ accelerated presentation
primarily asymptomatic
sx non-specific:
SOB
cough
sputum production
Dx of Silicosis
Chest CT preferred - better to differentiate from asbestosis
CXR
PFTs
Findings on CT for Silicosis
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
Silicosis treatment
no cure or definitive treatment
supportive:
bronchodilators, inhaled corticosteroids, pulm rehab, lung transplant
Silicosis complications
TB and non-tb mycobacterial infections**
Spontaneous pneumothorax
emphysema
lung cancer**
pulm HTN
resp failure
Silicosis prevention
best treatment is prevention
industrial intervention
PPE
screenings
smoking cessation
pneumo and flu vaccines in at risk pts
Asbestosis causative agent
asbestos (old home remodeling, heat, fire, chemically, electrical resistant material)
Direct toxic and macrophage activation -> inflammation -> fibrosis
Asbestosis dose dependent =
10-15 years post exposure
Asbestosis presentation
primarily asymptomatic
if sx they are non-specific:
SOB
non-productive cough **
fatigue
clubbing of digits - sign of hypoxia
bibasilar crackles
Dx Asbestosis workup
CT chest preferred
CXR
lung bx to confirm (rarely necessary)
PFTs for monitoring of progression
CT chest for Asbestosis shows
bilateral linear reticular opacities (honeycombing)
predilection of lower lungs
pleural plaques** (pathognomic)
Treatment for Asbestosis
no cure or definitive treatment
symptomatic relief
Asbestosis complications
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
Asbestosis prevention
annual lung cancer screening (low dose CT scan)
smoking cessation
flu and pneumococcal immunizations
Hypersensitivity Pneumonitis exposure to causative agent leads to
exposure to agent –> inflammation
aka extrinsic allergic alveolitis
Hypersensitivity Pneumonitis primarily manifests as
acute illness 4-8 hours after exposure
Symptoms of Hypersensitivity Pneumonitis
fever
chills
malaise
cough
dyspnea
nausea
PE for Hypersensitivity Pneumonitis
bibasilar crackles
resp distress:
tachycardia
tachypnea
+/- cyanosis
Hypersensitivity Pneumonitis workup
CXR - small nodular densities in the central lungs
CBC - elevated WBC count
check for antibodies to common substances
restrictive pattern on PFTs
Hypersensitivity Pneumonitis treatment
oral corticosteroids if severe
avoid further exposure
likely occupational change
Smoke inhalation 3 possible mechanisms of damage
- impaired Oxygenation – CO or cyanide - oxygen displacement
- upper airway thermal burns
- lower airway chemical injury or physical irritants
sign of inhalation injury
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
Smoking inhalation treatment
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
what can monitor infection from smoking inhalation daily
Sputum cultures
Prophylactic abx not indicated
