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interstitial and occupational lung disease Flashcards

1
Q

Does interstitial lung disease have an obstructive or restrictive pattern?

A

Restrictive

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2
Q

What are the two main symptoms of interstitial lung disease?

A
  • breathlessness

- dry cough

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3
Q

What are three common interstitial lung diseases?

A
  • idiopathic pulmonary fibrosis
  • extrinsic allergic alveolitis
  • sarcoidosis
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4
Q

Sarcoidosis:

  • what type of hypersensitivity reaction is involved?
  • what different systems are commonly (6)/less commonly involved (4)?
  • what does it cause to develop?
  • is it common in smokers or non-smokers?
A
  • Granulomatous type 4 hypersensitivity reaction of an unknown cause
  • common: lungs, lymph nodes, joints, liver, skin, eyes
  • less common: kidney, brain, nerves, heart
  • it causes a non-caseating granuloma of unknown aetiology
  • less common in smokers
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5
Q

What 6 clinical features can be found in acute sarcoidosis?

A
  • erythema nodosum
  • bilateral hilar lymphadenopathy
  • arthritis
  • uveitis
  • parotitis
  • fever
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6
Q

What 4 clinical features can be found in chronic sarcoidosis?

A
  • lung infiltrates (alveolitis)
  • skin infiltrations
  • peripheral lymphadenopathy
  • hypercalcaemia

(other organs: renal, myocardial, neurological, hepatitis, splenomegaly)

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7
Q

What are 4 differential diagnoses for sarcoidosis?

A
  • TB (tuberculin test -ve)
  • lymphoma
  • carcinoma
  • fungal infection
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8
Q

what is seen on chest x ray, CT scan lungs and tissue biopsy for sarcoidosis?

A

CXR: bilateral hilar lymphadenopathy
CT: peripheral nodular infiltrate
Tissue biopsy: non-caseating granuloma

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9
Q

What blood tests are indicative for sarcoid?

A

Angiotensin converting enzyme (ACE) levels as activity marker (not diagnostic test)

Raised calcium

Increased inflamm. markers

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10
Q

What is the treatment for acute v chronic sarcoid?

A

Acute - self limiting, usually no treatment unless vital affected and then steroids are used (eg impaired lung function, heart, eyes, brain, kidneys)

Chronic - oral steroids usually needed, immunosuppression(eg azathioprine, methotrexate, anti-TNF therapy)

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11
Q

What kind of follow up is needed for patients diagnosed with sarcoidosis?

A

-monitor CXR and pulmonary function for several years as often relapses

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12
Q

Extrinsic allergic alveolitis AKA hypersensitivity pneumonitis:

  • What type of hypersensitivty reaction is involved?
  • what different aetiologies exist?
A

-Type 3 hypersensitivity reaction to an antigen

Aetiologies:

  • thermophilic actinomycetes (farmers lung, malt workers, mushroom workers)
  • Avian antigens (bird fanciers lung)
  • drugs (gold, bleomycin, sulphasalazine)

No cause identified in about 30% cases

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13
Q

What are the clinical features of acute extrinsic allergic alveolitis?
What clinical signs are seen?
What is seen on CXR?
What is treatment?

A

-cough, breathless, fever, myalgia (Classically symptoms occur several hours after acute exposure (flu-like illness))

Signs: +/- pyrexia, crackles (no wheeze!), hypoxia

CxR: widespread pulmonary infiltrates

Treatment: oxygen, steroid and antigen avoidance

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14
Q

What are the clinical features of chronic extrinsic allergic alveolitis?
What clinical signs are seen?
What is seen on CXR?
What is seen on pulmonary function tests?

A

repeated low dose antigen exposure over time (years)
progressive breathlessness and cough

Signs: may be crackles, clubbing is unusual

CxR pulmonary fibrosis - most commonly in the upper zones

PFTs: restrictive defect (low FEV1 & FVC, high or normal ratio, low gas transfer - TLCO)

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15
Q

How is chronic extrinsic allergic alveolitis diagnosed? and what is the treatment?

A

Diagnosis: history of exposure, precipitins (IgG antibodies to guilty antigen), lung biopsy if in doubt.

Treatment: remove antigen exposure, oral steroids if breathless or low gas transfer.

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16
Q

Idiopathic pulmonary fibrosis:

  • what is the cause of primary IPF?
  • What are some causes of secondary IPF? (5)
A

Aetiology unknown.

Secondary causes:

  • Diseases e.g. Rheumatoid, SLE, systemic sclerosis, asbestos
  • Drugs e.g. amiodarone, busulphan, bleomycin, penicillamine, nitrofurantoin, methotrexate
17
Q

What are the clinical features of idiopathic pulmonary fibrosis (2)? Signs (2)? pulmonary function tests?

A
  • Progressive breathlessness of several years, dry cough
  • OE: clubbing, bilateral fine inspiratory crackles

PFTs: restrictive (reduced FEV1 and FVC = normal or raised FEV1/FVC ratio) reduced lung volumes, low gas transfer

18
Q

in idiopathic pulmonary fibrosis what is seen on CXR? and CT scan? is lung biopsy needed?

A

CxR - bilateral infiltrates;

CT scan - reticulonodular fibrotic shadowing, worse at the lung bases, and periphery. Traction bronchiectasis. Honey-combing cystic changes.

lung biopsy – not necessary if CT scan is diagnositic.

19
Q

What is the differential diagnosis for idiopathic pulmonary fibrosis? (7)

A

exclude occupational disease (asbestosis, silicosis), connective tissue disease (RhA, scleroderma, Sjogrens Disease, SLE), left ventricular failure, sarcoidosis, extrinsic allergic alveolitis.

(Ask about occupation (in depth), pets and drug history)

20
Q

How is idiopathic pulmonary diagnosed?

A

Diagnosis: combination of history, examination and radiology tests (HRCT scan)

If the presentation or the HRCT scan is atypical then lung biopsy (either transbronchial or thoracascopic) may be needed

21
Q

Describe the pathology seen in idiopathic pulmonary fibrosis

A

Usual Interstitial Pneumonia pattern (UIP) heterogenous fibrosis in alveolar walls with fibroblastic foci and destruction of architecture causing honeycombing. Inflammation is minimal.

22
Q

What is the treatment for idiopathic pulmonary fibrosis?

What is the prognosis?

A

Treatment is frustrating.
Steroids and immunosuppressants do not change course of disease
New antifibrotic drugs have emerged in recent years – PIRFENIDONE and NINTEDANIB – only therapies to have shown in randomised controlled trials to slow down disease progression BUT very expensive, and many side-effects.
Antifibrotic therapy does not reverse fibrosis, merely slows progression

Oxygen if hypoxic.

Lung transplantation in young patients

Prognosis: most patients progress within a few years into respiratory failure
Median survival of IPF is 4 years from point of diagnosis

23
Q

in coal workers pneumoconiosis what is the difference between simple and complex pneumoconiosis?

What two other clinical features are sometimes seen?

A

Simple pneumoconiosis - chest X-ray abnormality only (no impairment of lung function - often associated with chronic obstructive pulmonary disease).

Complicated pneumoconiosis - progressive massive fibrosis causing a restrictive pattern with breathlessness.

Also:
Chronic bronchitis (coal dust + smoking).

Caplan’s syndrome - rheumatoid pneumoconiosis (pulmonary nodules). This is where there is a combination of rheumatoid arthritis (RA) and pneumoconiosis that manifests as intrapulmonary nodules

24
Q

Silicosis:
How is this caused?
What is seen on CXR?
What is the difference between the simple pneumoconiosis and the chronic silicosis that is seen?

A

15-20 years exposure to quartz (eg mining, foundry workers, glass workers, boiler workers).

Simple pneumoconiosis – few symptoms; Chronic silicosis - restrictive pattern, pulmonary fibrosis.

chest X-ray abnormality (egg-shell calcification of hilar nodes).

25
Q

Asbestosis:

-Describe the four stages of the pleural disease caused?

A

1- Benign pleural plaques - asymptomatic

2- Acute asbestos pleuritis - fever, pain, bloody pleural effusion

3- Pleural Effusion and Diffuse pleural thickening - restrictive impairment

4- Malignant Mesothelioma - incurable pleural cancer. Presents with chest pain and pleural effusion. No available treatment - fatal within two years.

26
Q

Describe the pulmonary fibrosis seen in asbestosis:

  • how is it caused?
  • what is seen on pulmonary function tests?
  • What other tests are useful?
A

“Asbestosis” - heavy prolonged exposure.

Diffuse pulmonary fibrosis and restrictive defect.

Asbestos bodies in sputum. Asbestos fibres in lung biopsy.

27
Q

Apart from pleural malignancy what other malignancy does asbestos increase the risk of?

A

Bronchial carcinoma - asbestos multiplies risk in smokers

28
Q

For interstitial lung disease in general describe how the pathology of the lung progresses?

A
  • early stage is alveolitis (injury with inflammatory cell infiltration)
  • late stage is characterised by fibrosis
29
Q

What is the difference between transbronchial biopsy and thoracoscopic biopsy?

A

Transbronchial biopsy – special forceps used at bronchoscopy

Thoracoscopic biopsy – more invasive but more reliable and generates far more tissue

30
Q

What is idiopathic pulmonary fibrosis AKA?

A
  • cryptogenic fibrosing alveolitis

- usual interstitial pneumonia

31
Q

What is the pathology seen in idiopathic pulmonary fibrosis?

A

Subpleural and basal fibrosis

Inflammatory component variable

Terminally lung structure replaced by dilated spaces surrounded by fibrous walls

32
Q

What is pneumoconiosis? what are the three different types?

A

lung disease caused by mineral dust exposure:

  • asbestosis
  • coal workers lung
  • silicosis

Respiratory (17 decks)

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