Occupational lung disease - collins Flashcards

1
Q

What is pneumoconiosis

A

interstitial lung disease caused by particulate inhalation
- asbestos, silicosis, coal workers penumoconiosis (CWP) the big three

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2
Q

what does pneumoconiosis lead to

A

pulmonary fibrosis: inflammation -> scarring of the interstituium

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3
Q

What is black lung

A

coal workers pneumoconiosis - aka anthracosis, anthrasilicosis
carbon contraining particulate from coal mining

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4
Q

where are rates of CWP most common

A

central appalachia - kentucky, virginia and west virginia

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5
Q

what does the federal coal mine and health safety act do

A

established safety standards/inspection for coal mines
also funding for workers who develop CWP
reduced rates of CWP

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6
Q

what is the presentation of CWP

A

primarily asymptomatic
if symptoms develop: non-specific symptoms: SOB, cough, sputum production +/- black tinge, chest tightness

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7
Q

what is the first line diagnostic test for CWP

A

chest x-ray

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8
Q

what is seen on CXR with CWP

A

alveolar macrophages attempt to remove coal dust -> “coal macules”
2-5mm diffuse, small, round, nodular opacities on CXR
predilection for the upper lung, often with granular appearance

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9
Q

what are the diagnostic tests for CWP

A

CXR
PFTs on all - CWP produces minimal, if any, PFT changes - BUT coal dust can also cause chronic bronchitis and/or COPD
+/- Chest CT (more sensitive and specific)

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10
Q

What is the goal of treatment for CWP

A

identify CWP early through screening
screening via CXR including PFTs

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11
Q

what are the treatment options for CWP

A

no cure or definitive treatment
supportive treatment: bronchodilators, pulmonary rehabilitation, supplemental O2, smoking cessation, ? lung transplants

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12
Q

what are the complications of CWP

A

pulmonary HTN
Right sided HF
Respiratory failure
premature death

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13
Q

if abnormal screening test, how often are screenings from then on out

A

every 2 years

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14
Q

how often are routine normal screenings for CWP done

A

once every 5 years

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15
Q

how is CWP prevented

A

NIOSH set acceptable levels for coal dust in mines
use of PPE
avoid smoking/smoking cessation
encourage periodic screenings

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16
Q

What is silicosis

A

causative agent silica dust
M>F
exposure occurs during: manufacturing of glass, pottery, ceramics, bricks, concrete and artificial stone. abrasive blasting, foundry work, hydraulic fracturing, stone cutting, rock drilling, quarry work, tunneling
may be co-occuring with CWP

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17
Q

what is the presentation of chronic and accelerated silicosis

A

primarily asymptomatic, if symptoms develop, non-specific: SOB, cough, sputum production

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18
Q

What is the presentation of acute form of silicosis

A

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

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19
Q

how is silicosis diagnosed

A

Chest CT is preferred
+/- chest x-ray
PFTs for monitoring of progression

20
Q

why is Chest CT preferred for silicosis

A

better to differentiate from asbestosis
better to assess severity/progression
findings similar to CWP: 1-3mm small rounded opacities, mostly upper lungs, mediastinal and hilar lymphadenopathy, +/- lymph node calcifications

21
Q

what is seen with acute silicosis on chest CT

A

bilateral consolidation with ground glass opacities

22
Q

What are eggshell calcifications

A

lymph node calcifications

23
Q

what is the treatment of silicosis

A

no cure or definitive treatment
supportive treatment: bronchodilators, ICS, pulmonary rehab and ? lung transplant

24
Q

what are the complications of silicosis

A

TB and non-TB mycobacterial infections (30x increased risk)
spontaneous pneumothorax
emphysema
lung cancer
progressive massive fibrosis
pulmonary HTN
right sided HF
respiratory failure
premature death

25
what is the best treatment for silicosis
prevention
26
how do we prevent silicosis
primarily inducstrial interventions - isolation of risky activity, improved ventilation, changing to non-silica abrasives PPE screening of exposed patients Annual PPD screenings smoking cessation pneumococcal and flu vaccines
27
What is asbestosis
heat, fire, electricity and chemically resistant material occupational, passive and community exposures directly toxic and macrophage activation -> inflammation 10-15 years post exposure, dose-dependent
28
what populations are at risk of asbestosis
shipyard workers construction workers textile workers biomarkers sheet metal workers HVAC, plumbing and electrical workers other and anyone in home remodeling/building
29
what is the presentation of asbestosis
primarily asymptomatic non-specific: SOB, nonproductive cough, fatigue, clubbing on digits (sign of hypoxia), babasilar crackles
30
how do you diagnose asbestosis
chest CT preferred +/- CXR lung biopsy to confirm (rarely necessary) PFTs for monitoring of progression
31
what is seen on Chest CT with asbestosis
bilateral linear reticular opacities ('honeycombing') predilection for the lower lobes pleural plaques (pathognomonic)
32
What is the treatment for asbestosis
no cure or definitive treatement (symptomatic)
33
what are the complications of asbestosis
lung cancer: Mesothelioma, non-small cell lung cancer (NSCLC) - 8-10x increased risk pulmonary HTN Right sided HF respiratory failure premature death
34
What is mesothelioma
mainly caused by asbestos, roughly 3,000 cases per year
35
how is asbestosis prevented
asbestoses abatement (precautions to limit fiber disruption) annual lung cancer screening - low dose CT scan smoking cessation flu and pneumococcal immunization
36
what is another name for hypersensitivity pneumonitis
AKA extrinsic allergic alveolitis
37
what is hypersensitivity pneumonitis
exposure to antigen - inflammatory response over 300+ substances linked to the disease peak incidence: 50-55
38
what is the presentation of hypersensitivty pneumonitis
primarily manifests as acute illness 4-8 hours after exposure fever, chills, malaise, cough, dyspnea, nausea
39
what is seen on physical exam with hypersensitivity pneumonitis
bibasilar crackles tachycardia tachypenia +/- cyanosis
40
how is hypersensitivity worked up
CXR - small nodular densities in central lungs CBC - elevated WBC, increased in band cells (left shift) check for antibodies to common substances would see restrictive pattern on spirometry
41
what is the treatment of hypersensitivity pneumonitis
oral corticosteroids if severe avoid further exposure likely occupational change
42
what is a pulmonary complication in as many as 1/3 of in patient burn patients
smoke inhalation
43
what are the mechanisms of damage from smoke inhalation
impaired oxygenation (CO or cyanide -> oxygen displacement) upper airway thermal burns lower airway chemical injuries or physical irritants
44
what are the signs of inhalation injury
occurred in enclosed space signed nasal hair or burns on lips deep or full-thickness burn to face, neck, upper torso black-colored sputum or soot around nasal passages
45
what are the upper airway injuries with smoking inhalation
heat related more rapid presentation (18-24h) may lead to tissue edema, inability to clear secretions and airway obstructioni inspiratory stridor evaluation with laryngoscope/Bronchoscope
46
what are lower airway injuries with smoke inhalation
chemical burns inhalation of products of combustion may worsen over 24-72 hours produces bronchospasm and sputum see dyspnea, tachypnea, labored breathing, cyanosis diffuse wheezing and ronchi on PE
47
what are the complication of lower airway smoke inhalation injuries
ARDS (day 1-2) sloughing of bronchiolar mucosa -> obstruction, hypoxia, atelectasis (day 2-3) bacterial infection-> PNA (day 5-7)