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Respiratory 4 > Occupational and Environmental Lung diseases > Flashcards

Occupational and Environmental Lung diseases Flashcards

1
Q

General Considerations of Occupational and Environmental lung diseases?

A

A worldwide problem – Diverse group of diseases Exposures are a major cause of respiratory diseases

Lung diseases caused by inhalation of particular matter or gases and fumes in the workplace or environment

Site of deposition of inhaled matter in the respiratory tract is dependent upon water solubility for gases and fumes and particle size for solids

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2
Q

History of the patient with occupational/environmental lung disease?

A
  1. Medical history
  2. Occupational history All jobs held past to present, job details/work environment, how long worked at the job
  3. Environmental history
  4. Pets
  5. Hobbies
  6. Travel history
  7. Social history
  8. Smoking history
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3
Q

Approach to a patient with suspected occupational/environmental?

A
  • Physical exam
  • PFT – Spirometry, lung volume, DLCO – ± Bronchoprovocation test
  • Radiology imaging: – Chest x-ray, – CT thorax
  • Lab – ± Serology studies, and skin test depending upon disease under consideration

Ask yourself Why did this patient develop this illness? Is there an intervention to prevent disease progression

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4
Q

What factors play into occupational/environmental exposure?

A
  1. Where deposition occurs with the respiratory tract
  2. Concentration of material retained
  3. Dose of exposure
  4. Physical and chemical properties of the matter
  5. Host susceptibility: Anatomy of the airway, Clearance mechanism, Genetic make up of the host, Immune status, Underlying/coexisting lung disease
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5
Q

For gases and fumes what deteremines level of penetration? For particular matter what determines the level of deposition?

A

For gases/fumes solubility determines level of penetration

High soluble gases are trapped in the moist lining of the upper airway
Low soluble gases can reach the lower lung parenchyma down to the alveoli

For particular matter the particle size or aerodynamic diameter is of greatest importance in determining the level of deposition Inhaled particles of dust <5mm can reach the terminal bronchioles and alveoli

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6
Q

List the different gases and where they deposit based off of where they go in the lung?

A
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7
Q

Pulmonary disease is related to?

A

Pulmonary disease risk is related to the total burden of inhaled particles.

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8
Q

Toxic inhalation lung injury? Due to? Level of deposition depends on? Pathologically dependent on?

A

Due to chemical release into the atmosphere as gases, fumes or mist

Level of deposition in the respiratory tract depends on the chemicals water solubility High: Nose and oropharynx Intermediate: Trachea, upper lung zone, bronchi Low: Lower lung, bronchioles, and alveoli

Pathologically dependent on physical properties of inhaled substance and host factors

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9
Q

What is Silo Filler’s Disease? Different ppm of nitrogen oxides and what they manifest to?

A

Oxides of nitrogen (primarily NO2) releases as a byproduct of decomposing silage, typically corn or alfalfa

Oxides of nitrogen low water solubility putting the lower respiratory tract at risk

15-25 ppm: Acute mucous membrane irritation eyes and throat

25-100 ppm: Toxic pneumonitis and bronchiolitis often with smothering sensation and dyspnea

>150 ppm: Often fatal obstructive bronchiolitis, chemical pneumonitis, and pulmonary edema

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10
Q

Symptoms of Silo Filler’s? Treatment?

A

Symptom onset may be delayed, hours after exposure patients may develop severe pulmonary edema resembling ARDS

Relapse 3-6 weeks after initial exposure cough, chills, fever, dyspnea

Treatment: Removal from the environment Consider corticosteroids

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11
Q

Air pollution can be caused by?

A

Air pollution can be caused by a wide range of substances in the environment. Particulate matter and volatile organic compounds are the major contributors.

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12
Q

Air pollution can lead to?

A
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13
Q

Explain indoor air pollution?

A
  • Common in developing countries where around 3 billion people use biomass fuels for heating and cooking
  • Over 4 million premature deaths attributed from cooking with solid fuels: Wood, charcoal, crop residues, dung
  • More than 50% f premature deaths due to pneumonia among children under 5 caused by particulate matter

4.3 million people a year die premature from illness attributable to household air pollution due to biomass fuels for cooking • 12% are due to pneumonia • 34% are due to stroke • 26% from ischemic heart disease • 22% from chronic obstructive pulmonary disease (COPD) • 6%% from lung cancer

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14
Q

What is Pneumoconiosis?

A

Derived from the Greek term Pneumo meaning “Breath” And Konis meaning “Dust”

Fibrotic lung diseases following inhalation of inorganic dust

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15
Q

What are the three major types of Pneumoconiosis?

A
  • Silicosis
  • Coal Worker’s Pneumoconiosis
  • Asbestosis and other asbestos related lung disease
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16
Q

What is Silicosis?

A

Most prevalent chronic occupational disease worldwide

A diffuse parenchymal lung disease due to exposure to silica (quartz)

Pattern of disease depends on intensity of exposure and duration

Pathology cytotoxic effect of silica on alveolar macrophage

Hallmark lesion silicotic nodule (small)

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17
Q

What are the three forms of Silicosis?

A
  1. Chronic (10-20 years after exposure)
  2. Accelerated (<10 years after exposure) Change similar to chronic but more intense
  3. Acute (weeks to 4-5 years) Classic example: sandblasting
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18
Q

Explain chronic Silicosis?

A

Silicotic nodule

Lower dust concentration than accelerated or acute

single chronic silicosis nodules can coalesce and lead to complicated chronic complicated nodules which coalesce to large mass (PMF)

PMF progressive massive fibrosis

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19
Q

Chest x-ray of Silicosis? for chronic? Accelerated? Acute?

A

Chronic disease: 1°involves upper lung zones

Nodules can coalesce → large masses spoken of as Progressive Massive Fibrosis (PMF) May see “egg shell calcification” in hilar lymph nodes

Chest x-ray: Accelerated similar to chronic

Chest x-ray: Acute mid-lower lung zone ground-glass opacities

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20
Q

Increased risk for what with Silicosis? Treatment? Prevention? Example occupations?

A

Increased risk for: 1. Lung cancer 2. M. Tuberculosis and Atypical Mycobacterium 3. Rheumatoid Arthritis and Systemic Sclerosis

Treatment: None

Prevention Management: Prevention minimize exposure

Example Occupations: Mining, tunneling, quarrying, sandblasting, glass workers

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21
Q

Coal workers Pneumoconiosis Features?

A

Disease resulting from chronic exposure to coal and dust

Severity of CWP corresponds to levels of coal and dust exposure and carbon content (highest: anthracite coal)

Carbon dust tends to be less fibrogenic than silica (quartz)

Coal dust engulfed by macrophage leads to inflammation which leads to fibrosis

Coal macules (small nodules) favor upper lung zones

CWP better defined by HRCT compared to CXR

22
Q

Pathogenesis of Coal workers pneumonconiosis?

A

1° lesion is the coal macule distributed mainly in both upper lobes. The lesion consists of aggregates of dust laden macrophages and fibroblasts in the respiratory bronchioles and alveoli. It can weaken the bronchioles and cause focal emphysema. Hard coal (anthracite) > soft coal (bituminous)

23
Q

What are the two types of Coal workers Pneumoconiosis?

A

Simple pneumoconiosis not associated with resp symptoms

Complicated/Progressive massive fibrosis Densities larger than 1-2 cm in size

24
Q

What are complications of Coal Workers Pneumoconiosis (CWP)? What is Caplan Syndrome?

A

Complications
Mycobacterium tuberculosis and atypical mycobacteria but less frequently than in silicosis

Caplan Syndrome: Association of CWP with seropositive rheumatoid arthritis Large pulmonary rheumatoid nodules associated with CWP Nodules may be multiple and may cavitate

25
Q

Asbestos related lung diseases?

A
  • Widely used because of its thermal and fire resistance
  • Over 3000 commercial uses – A significant health concern: A well-recognized human carcinogen
  • Estimated 27 million workers exposed between 1940-1975
  • Long latency period between fiber exposure and development of asbestosis or mesothelioma
26
Q

What are the classses of Asbestos?

A

Asbestos: A group of naturally occurring hydrated silicate fibers 2 Classes of asbestos fibers

  1. Serpentine (chrysotile): Curly stranded curved structures 95% of all asbestos used commercially (low malignancy risk)
  2. Amphibole (crocidolite, amosite, and tremolite): straight, rod-like fibers (high malignancy risk)
    All types cause asbestosis, pleural plaques, pleural effusion, Mesothelioma, and lung cancer
27
Q

What are the mechanisms of exposure to asbestos exposure?

A
  1. Occupational Majority of cases Example: mining/mining of asbestos, shipbuilding, boiler work, brake lining
  2. Para-occupational Relatives of asbestos workers exposed to “carry home” asbestos in clothes
  3. Environmental Mining communities with ore contaminants with asbestos geological exposure from natural deposits
28
Q

Types of Asbestos injuries?

A
  • Asbestosis
  • Benign asbestos-related pleural disease – Pleural plaques esp. mid to lower lateral pleura and hemidiaphragm with calcification – Pleural effusion – Diffuse pleural thickening – Rounded atelectasis (combined pleura and parenchyma)
  • Lung cancer (all cell types but especially bronchogenic)
  • Mesothelioma – pleural malignancy
29
Q

What is Asbestosis?

A
  • A diffuse parenchymal lung disease/ILD due to asbestos exposure
  • Disease development relates to degree and length of exposure
  • Requires much higher dose of asbestos than the minimum necessary to cause mesothelioma and benign pleural disease
  • Long latency period (years)
  • Increased incidence of lung cancer with 60% increase in smokers
30
Q

What are the clinical features of Asbestosis? CXR? HRCT? PFT’s?

A

Insidious onset of dyspnea, non-productive cough, bibasilar crackles, clubbing in 40% of cases

CXR: Reticulonodular pattern 1°lower lobes of lung
Pleural plaques and/or thickening may progress to honeycombing

HRCT: Ground-glass opacities and above

PFT: Restrictive pattern decreased FVC, FEV1/FVC Normal, TLC decreased, DLCO decreased.

31
Q

What is the pharmacologic treatment of Asbestosis?

A

No pharmacologic treatment

Supportive: smoking cessation, flu shot, pneumococcal vaccination

Primary prevention

32
Q

Pathology of Asbestos?

A

Asbestos fibers penetrate macrophage and pulmonary epithelial cells around respiratory bronchioles causing an inflammatory response that progresses to peribronchiolar fibrosis

33
Q

The effect of asbestos exposure and smoking on the risk of lung cancer?

A
34
Q

Summarize CWP, Silicosis, and Asbestosis?

A
35
Q

Explain Mesothelioma aka Malignant Pleural Mesothelioma?

A
  • A rare malignant tumor of the parietal pleura or peritoneum resulting from asbestos exposure
  • Smoking NOT a risk factor
  • Not asbestos dose related
  • Long latency period between exposure and diagnosis (±40 years)
36
Q

Clinical Features of Mesothelioma?

A
  • Chest pain (usually dull), slowly progressive shortness of breath, weight loss, fatigue
  • Paraneoplastic syndromes can occur: DIL, hemolytic anemia, hypoglycemia, hypercalcemia
  • Pleural effusion in 60% of patients
  • CXR: Irregular or lobulated pleural thickening
  • Diagnosis: Pleural disease
  • Very poor prognosis no really good treatment options
37
Q

explain Hypersensitivity Pneumonitis (HP) (Extrinsic Allergic Alveolitis)?

A

A group of diffuse parenchymal lung diseases caused by inhalation of organic or inorganic antigens

Fungi → Farmer’s lung wood pulp Worker’s lung

Animal protein – Bird Fancier’s disease

Bacteria (thermophilic actinomycetes – Farmer’s lung)

Chemicals – Isocyanate HP, Amiodarone

Divided into acute, subacute, and chronic forms Based on time, course of presentataion, and intensity of antigen exposure

38
Q

Pathology of Hypersensitivity Pneumonitis?

A

Immunologic disease involving T lymphocytes Localize to the alveoli and distant bronchioles

Type IV hypersensitivity (granuloma formation) and Type III Antibody-antigen immune complex

39
Q

Clinical Features of Hypersensitivity Pneumonitis?

A

Variable: Depends on state of the disease

Acute: Abrupt onset chills, fever, athralgias, myalgias, SOB, dry cough, chest tightness, bibasilar crackles

Subacute and Chronic: Progressive SOB, productive cough, weight loss, fatigue

40
Q

What do the labs, Bronchoalveolar lavage, HRCT, and PFT show for hypersensitivity pneumonitis?

A

Lab: Acute disease leukocytosis not eosinophilia non-specific serum markers of inflammation CRP, ESR, LDH, ACE

BAL: Lymphocytic alveolitis Serum precipitins neither specific nor sensitive for HP but in right clinical context for HP may help to confirm Imaging:

HRCT most sensitive may demonstrate groundglass opacities, centrilobular nodules, mosaic attenuation, reticulation, honeycombing

PFT: Restriction

41
Q

Diagnosis of Hypersensitivity Pneumonitis? Treatment?

A

Ideally history of antigen exposure typical clinical and HRCT feature

Treatment Early diagnosis and elimination/avoidance of antigen Occupational and environmental history very important Oral corticosteroids are the first-line treatment used at all Stages of the disease In patient with progressive fibrotic HP lung transplantation should be considered

42
Q

Prognosis of Hypersensitivity Pneumonitis?

A

Highly variable depends upon number of factors type and duration of antigen exposure and the host immune response Can after repeat exposures cause chronic respiratory failure

43
Q

What is Occupational airway disease (occupational asthma)?

A

New onset of variable airflow limitation and/or bronchial hyperresponsiveness due to workplace environment exposure in an individual with no prior history of asthma

44
Q

What is work related asthma?

A

Pre-existing asthma aggravated by the work environment

45
Q

What are the classifications of occupational airway disease based on pathophysiology?

A
  1. Immunologic – allergic Latency: weeks to decades IgE mediated Non IgE mediated
  2. Non-immunologic (irritant induced) Non-latency Acute onset: high level of irritant exposure – Single episode RADS (Respiratory Airway Dysfunction Syndrome) – Multiple episodes Delayed onset: moderate irritant exposure
46
Q

Examples of things/occupations causing occupational asthma?

A

High molecular weight Flour Bakery worker

Low molecular weight Wood Saw mill worker

47
Q

What things should be done to diagnose occupational asthma?

A
  1. History Extremely important Temporal association of symptoms with work Decreased away from work
  2. Peak flow monitoring before during after work
  3. PFT
  4. Physical exam wheezing
  5. Allergy test skin test and immunologic (IgE assessment)
  6. Bronchoprovocation test
48
Q

Management of Occupational asthma?

A
  1. Remove or limit the patient from irritating agent in the workplace environment
  2. Pharmacologic medications
49
Q

What is reactive airways dysfunction syndrome?

A

Persistence of airway hyperresonsiveness/reactivity Following an acute exposure to a respiratory irritant

  • Onset within 24 hours of exposure and persistence for at least 3 weeks
  • Non-immunologic (irritant induced)
  • No latency
  • Symptoms consistent with asthma (cough, wheeze, dyspnea)
  • Non-smoker
50
Q

Agents responsible for Reactive Airways Dysfunctional Syndrome?

A

Respiratory 4 (18 decks)

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