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Clin Med2: Pulmonology > Occupational lung disease - collins > Flashcards

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
Q

what is the best treatment for silicosis

A

prevention

26
Q

how do we prevent silicosis

A

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
Q

What is asbestosis

A

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
Q

what populations are at risk of asbestosis

A

shipyard workers
construction workers
textile workers
biomarkers
sheet metal workers
HVAC, plumbing and electrical workers
other and anyone in home remodeling/building

29
Q

what is the presentation of asbestosis

A

primarily asymptomatic
non-specific: SOB, nonproductive cough, fatigue, clubbing on digits (sign of hypoxia), babasilar crackles

30
Q

how do you diagnose asbestosis

A

chest CT preferred
+/- CXR
lung biopsy to confirm (rarely necessary)
PFTs for monitoring of progression

31
Q

what is seen on Chest CT with asbestosis

A

bilateral linear reticular opacities (‘honeycombing’)
predilection for the lower lobes
pleural plaques (pathognomonic)

32
Q

What is the treatment for asbestosis

A

no cure or definitive treatement (symptomatic)

33
Q

what are the complications of asbestosis

A

lung cancer: Mesothelioma, non-small cell lung cancer (NSCLC) - 8-10x increased risk
pulmonary HTN
Right sided HF
respiratory failure
premature death

34
Q

What is mesothelioma

A

mainly caused by asbestos, roughly 3,000 cases per year

35
Q

how is asbestosis prevented

A

asbestoses abatement (precautions to limit fiber disruption)
annual lung cancer screening - low dose CT scan
smoking cessation
flu and pneumococcal immunization

36
Q

what is another name for hypersensitivity pneumonitis

A

AKA extrinsic allergic alveolitis

37
Q

what is hypersensitivity pneumonitis

A

exposure to antigen - inflammatory response
over 300+ substances linked to the disease
peak incidence: 50-55

38
Q

what is the presentation of hypersensitivty pneumonitis

A

primarily manifests as acute illness 4-8 hours after exposure
fever, chills, malaise, cough, dyspnea, nausea

39
Q

what is seen on physical exam with hypersensitivity pneumonitis

A

bibasilar crackles
tachycardia
tachypenia
+/- cyanosis

40
Q

how is hypersensitivity worked up

A

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
Q

what is the treatment of hypersensitivity pneumonitis

A

oral corticosteroids if severe
avoid further exposure
likely occupational change

42
Q

what is a pulmonary complication in as many as 1/3 of in patient burn patients

A

smoke inhalation

43
Q

what are the mechanisms of damage from smoke inhalation

A

impaired oxygenation (CO or cyanide -> oxygen displacement)
upper airway thermal burns
lower airway chemical injuries or physical irritants

44
Q

what are the signs of inhalation injury

A

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
Q

what are the upper airway injuries with smoking inhalation

A

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
Q

what are lower airway injuries with smoke inhalation

A

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
Q

what are the complication of lower airway smoke inhalation injuries

A

ARDS (day 1-2)
sloughing of bronchiolar mucosa -> obstruction, hypoxia, atelectasis (day 2-3)
bacterial infection-> PNA (day 5-7)

Clin Med2: Pulmonology (13 decks)

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