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Respiriatory: Airway Disease > Interstitial and Occupational Lung Disease > Flashcards

Interstitial and Occupational Lung Disease Flashcards

1
Q

What is interstitial disease?

A

Any disease affecting the lung interstitium (e.g. alveoli, terminal bronchi)

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2
Q

What are the effects of interstitial lung disease?

A
  • Interferes with gas transfer

* Restrictive lung pattern

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3
Q

What are symptoms of interstitial disease?

A
  • Breathlessness (mainly on exertion)

* Dry cough

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4
Q

What are types of interstitial lung disease?

A
  • Acute
  • Episodic
  • Chronic
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5
Q

What is chronic interstitial lung disease?

A
  • Part of systemic disease
  • Exposure to agent (e.g. drug, dust etc)
  • Idiopathic - no known cause
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6
Q

What are 3 types of interstitial lung disease?

A
  • Granulomatous diseases e.g. sarcoidosis, extrinsic allergic alveolitis
  • Idiopathic pulmonary fibrosis (IPF)
  • Non-specific interstitial pneumonia (NSIP)
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7
Q

What is sarcoidosis?

A

Granulomatous type 4 hypersensitivity disease of unknown cause

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8
Q

What systems are involved in sarcoidosis?

A
  • Common: lungs, lymph nodes, joints, liver, skin, eyes

* Less common: kidneys, brain, nerves, heart

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9
Q

What is the pathology of sarcoidosis?

A
  • Non-caseating granuloma of unknown aetiology

* Imbalance of immune system with type 4 (cell mediated) hypersensitivity

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10
Q

What is unusual about the prevalence of sarcoidosis?

A

Less common in smokers

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11
Q

What are clinical features of acute sarcoidosis?

A
  • erythema nodosum
  • bilateral hilar lymphadenopathy
  • arthritis
  • uveitis
  • parotitis (inflammation of parotid glands)
  • fever
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12
Q

What are the clinical features of chronic sarcoidosis?

A
  • lung infiltrates (alveolitis)
  • skin infiltrations
  • peripheral lymphadenopathy
  • hypercalcaemia
  • Other organs: renal, myocardial, neurological, hepatitis, splenomegaly
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13
Q

What are differential diagnoses of sarcoidosis?

A
  • Tuberculosis
  • Lymphoma
  • Carcinoma
  • Fungal infection
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14
Q

What are possible investigations for sarcoidosis?

A
  • CXR (BHL) - primary test, often diagnostic
  • CT scan of lungs (peripheral nodular infiltrate)
  • Tissue biopsy (non-caveating granuloma)
  • Pulmonary function (restrictive pattern due to lung infiltrates)
  • Blood test - Agiotensin Converting Enzyme (ACE) as activity marker (NOT diagnostic test), hypercalcaemia, increased inflammatory markers)
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15
Q

What is the treatment for acute and chronic sarcoidosis?

A
  • Acute: self-limiting condition - usually no treatment (oral steroids if vital organ affected e.g. impaired lung function, brain, eyes, heart, kidneys)
  • Chronic: oral steroids usually needed, immunosuppression (e.g. azathioprine, methotrexate, anti-TNF therapy)
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16
Q

Why do CXR and pulmonary function have to be monitored for several years after sarcoidosis diagnosis?

A

Often relapses

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17
Q

Why is it important to treat uveitis due to sarcoidosis with steroid drops?

A

If don’t control uveitis, anterior chamber of eye fills up with inflammatory fluid, leading to glaucoma and long term damage

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18
Q

What are non-caseating granulomas in sarcoidosis composed of?

A

Epithelioid histiocytes, multinucleate giant cells, lymphocytes, plasma cells, fibroblasts and collagen

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19
Q

What is extrinsic allergic alveolitis (hypersensitivity pneumonitis)?

A

Type II hypersensitivity (immune complex deposition) reaction to antigen - inflammation of the alveoli

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20
Q

What is another name for extrinsic allergic alveolitis?

A

Hypersensitivity pneumonitis

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21
Q

What is the aetiology of extrinsic allergic alveolitis?

A
  • Thermophillic actinomycetes (farmer’s lung, malt workers, mushroom workers)
  • Avain antigens (bird fancier’s lung)
  • Drugs (gold, bleomycin, sulphasalazine)
  • No cause identified in 30% of cases
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22
Q

How is hypersensitivity reaction causes in extrinsic allergic alveolitis?

A
  • Immune complexes form
  • Circulate in bloodstream
  • Become deposited in lungs causing hypersensitivity reaction
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23
Q

What are the 2 classifications of EAA?

A

Acute or chronic

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24
Q

What are the symptoms of acute EAA?

A
  • Cough
  • Breathlessness
  • Fever
  • Myalgia
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25
Q

When do symptoms of acute EAA normally appear?

A

Several hours after antigen exposure (flu-like illness)

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26
Q

What are the clinical signs of acute EAA?

A
  • Pyrexia
  • Crackles (no wheeze)
  • Hypoxia
  • On CXR, will see widespread pulmonary infiltrates
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27
Q

What is the treatment for acute EAA?

A
  • Oxygen
  • Steroids
  • Antigen avoidance
28
Q

What is chronic EAA?

A

Repeated low dose antigen exposure over years

29
Q

What are the symptoms of chronic EAA?

A

Progressive breathlessness and cough

30
Q

What are the clinical signs of chronic EAA?

A
  • Crackles
  • Finger clubbing (unusual but possible)
  • On CXR, will see pulmonary fibrosis, most commonly in the upper zones
  • Pulmonary function tests will show low FEV1 and FVC, low gas transfer - TLCO)
31
Q

What further tests can help diagnose chronic EAA?

A
  • History of exposure
  • Precipitins (measure IgG antibodies specific to antigen)
  • Lung biopsy
32
Q

What is the treatment for chronic EAA?

A
  • Remove antigen exposure

* Oral steroids if breathless or low gas transfer

33
Q

What is Idiopathic Pulmonary Fibrosis?

A

The most common interstitial lung disease

34
Q

What is the aetiology of idiopathic pulmonary fibrosis?

A 
Idiopathic 
However, several possible causes
* Imbalance of fibrotic repair system
* Possibly related to gastric reflux
* IPF NOT an inflammatory disease
* More common in smokers
35
Q

What are other causes of pulmonary fibrosis (other than IPF)?

A
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Systemic sclerosis
  • Asbestos
  • Drugs: amiodarone, busulphan, bleomycin, penicillamine, nitrofurantoin, methotrexate
36
Q

What are the clinical presentations of IPF?

A
  • Progressive breathlessness over several years
  • Dry cough
  • Finger clubbing
  • Bilateral fine inspiratory crackles
  • Restrictive pattern on PFTs, reduced lung volume, low gas transfer
  • CXR shows bilateral infiltrates
  • CT scan - reticulonodular fibrotic shadowing, worse at lung bases and periphery, traction bronchiectasis and honey-combing cystic changes
37
Q

What are differential diagnoses for idiopathic pulmonary fibrosis?

A
  • Occupational disease (asbestosis, silicosis)
  • Connective tissue disease (RhA, scleroderma, Sjogrens Disease, SLE)
  • Left ventricular failure
  • Sarcoidosis
  • Extrinsic allergic alveolitis
38
Q

How is a diagnosis is idiopathic pulmonary fibrosis reached?

A
  • History (ask about occupation, pets and drug history)
  • Examination
  • Radiology tests (HRCT scan)
39
Q

What is done if the presentation or the HRCT scan is atypical in IPF?

A

Lung biopsy (either transbronchial or thoracascopic) carried out

40
Q

What is the pathology of idiopathic pulmonary fibrosis?

A
  • Unusual interstitial pneumonia pattern (UIP)
  • Heterogenous fibrosis in alveolar walls
  • Fibroblastic foci
  • Destruction of architecture causing honeycombing
  • Very little inflammation as NOT an inflammatory disease
41
Q

What is the treatment for IPF?

A
  • Steroids and immunosuppressants - do not change course of the disease
  • Antifibrotic drugs (Pirfenidone and Nintedanib) - only therapies which have shown to slow down disease progression
  • Oxygen if hypoxic
  • Lung transplantation in patients under 65
42
Q

What are the drawbacks of antifibrotic drugs in IPF?

A
  • Antifribotic therapy does not reverse fibrosis, merely slows down progression
  • Very expensive
  • Many side-effects
43
Q

What is the prognosis of those with IPF?

A

Most patients progress into respiratory failure within a few years

44
Q

What is the median survival of IPF?

A

4 years after diagnosis

45
Q

What are the 2 classes of coal workers pneumoconiosis?

A
  • Simple pneumoconiosis

* Complicated pneumoconiosis

46
Q

What is simple pneumoconiosis?

A

CXR abnormality - no impairment of lung function, often associated with chronic obstructive pulmonary disease (COPD)

47
Q

What is complicated pneumoconiosis?

A

Progressive massive fibrosis - restrictive pattern with breathlessness

48
Q

What are the causes of chronic bronchitis?

A

Coal dust + smoking

49
Q

What are the causes of Caplan’s syndrome?

A

Rheumatoid arthritis + coal dust, causes pulmonary nodules in lungs

(Also called rheumatoid pneumoconiosis)

50
Q

What is silicosis?

A

Occupational lung disease caused by 15-20 years exposure to quarts (e.g. mining, foundry workers, glass workers, boiler workers)

51
Q

What conditions can exposure to silica (SO2) lead to?

A
  • Simple pneumoconiosis - few symptoms

* Chronic silicosis - restrictive pattern, pulmonary fibrosis

52
Q

What abnormalities are found on a CXR of someone with simple pneumoconiosis?

A

Egg-shell calcification of hilar nodes

53
Q

What is seen on a CXR of someone with complicated pneumoconiosis?

A

Balls of fibrous tissue that appear like cancer

54
Q

What is baritosis?

A

Pneumoconiosis that is caused by long-term exposure to barium dust

55
Q

What is the appearance of baritosis on a CXR?

A

Will appear very dense (barium often used for x-ray investigations due to density)

56
Q

What occupations are most at risk of asbestos-related lung disorders?

A

Mining, construction, shipbuilding, boilers and piping, automative components (e.g. brake linings)

57
Q

What is the most common condition caused by asbestos exposure?

A

Benign pleural plaques (pleural disease)

58
Q

What are examples of asbestos-related lung disorders?

A
  • Pleural disease - benign pleural plaques, acute asbestos pleuritis, pleural effusion and diffuse pleural thickening, malignant mesothelioma
  • Pulmonary fibrosis - “asbestosis”
  • Bronchial carcinoma - asbestos multiplies risk in smokers
59
Q

What is the meaning of “diffuse” when referring to a medical condition?

A

Not localised - can spread widely

60
Q

What are examples of pleural disease caused by asbestos exposure?

A
  • Benign pleural plaques - asymptomatic
  • Acute asbestos pleuritis - fever, pain, bloody pleural effusion
  • Pleural effusion and diffuse pleural thickening - restrictive impairment
  • Malignant mesothelioma - incurable pleural cancer
61
Q

What are clinical presentations of malignant mesothelioma?

A

Chest pain and pleural effusion

62
Q

What is the treatment for malignant mesothelioma?

A

No cure available - chemotherapy can be used to slow down progression, usually fatal within 2 years

63
Q

What causes asbestosis?

A

Heavy prolonged exposure to asbestos

64
Q

What is asbestosis?

A

Pulmonary fibrosis caused by prolonged asbestos exposure

65
Q

What are clinical features of asbestosis?

A
  • Diffuse pulmonary fibrosis
  • Restrive pattern on PFT
  • Asbestos bodies in sputum
  • Asbestos fibres in lung biopsy
66
Q

Why must you be thorough when checking history for asbestos exposure?

A

Exposure to asbestos may not be obvious - could be a school teacher (school buildings previously riddled with asbestos)

Respiriatory: Airway Disease (10 decks)

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