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Respiratory 2 > Interstitial Lung Disease > Flashcards

Interstitial Lung Disease Flashcards

1
Q

Interstitial Lung Disease

A

Broad term describing a range of lung disorders that affect the interstitium (the area around the alveoli) of the lung.

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2
Q

What are some of the known causes of interstitial lung disease?

A 
Drugs e.g those used in chemotherapy.
CTD 
Asbestosis
Pneumoconiosis
HP
Idiopathic (2/3 cases)
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3
Q

CTD

A

Connective tissue disease-associated interstitial lung disease e.g scleroderma or systemic sclerosis.

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4
Q

What are the characteristics of interstitial lung disease and what are there symptoms?

A

They are characterised by varying degrees of inflammation and fibrosis, initially affecting the interstitium of the lung, which typically present with exertional dyspnoea, with or without cough.

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5
Q

In a patient with ILD what would you hear on auscultation and why?

A

Crackles due to pulmonary fibrosis.

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6
Q

What are the steps taken when investigating suspected ILD?

A 
History
Physical examination
Blood serum tests
Lung function tests
Radiology (HRCT - high resolution CT)
Lung biopsy in some cases.
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7
Q

What is the purpose of blood tests when investigating ILD?

A

• Blood tests , including antinuclear antibodies (ANA) and rheumatoid factor (RF), are performed to exclude autoimmune rheumatic disease but there is no specific serological test for IPF.

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8
Q

Asbestosis

A

An ILD characterised by slowly progressive, diffuse pulmonary fibrosis caused by inhalation of asbestos fibres.

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9
Q

What are the symptoms of asbestos?

> what is important to take into account when thinking of asbestosis?

A

Insidious onset of breathlessness with exertion, which progresses even in the absence of further asbestos exposure.
> Has a latency period of 20/30years important to think about risk factors e.g exposure to asbestos in work.

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10
Q

What is the treatment for asbestosis?

A

No specific treatment for asbestosis.
o Avoidance of any further asbestos exposure
o Supportive care

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11
Q

What are the complications associated with asbestosis?

A

Increased risk of respiratory failure and lung cancer.

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12
Q

Hypersensitivity Pneumonitis

A

A form of ILD that is caused by an immunologic reaction to an inhaled agent/organic antigen within the pulmonary parenchyma.

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13
Q

What is the pathological pattern of acute interstitial pneumonia?

A

Diffuse alveolar damage

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14
Q

What is the most common cause of idiopathic interstitial pneumonias?

A

Idiopathic pulmonary fibrosis (IPF) is the most common of the idiopathic interstitial pneumonias.

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15
Q

What is the histological appearance of idiopathic pulmonary fibrosis?

A

Usual interstitial pneumonia (UIP) is the histological finding in IPF. The key feature is a heterogenous appearance with areas of normal lung punctuated by areas of marked fibrosis, honeycombing mainly in subpleural areas.

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16
Q

What is the pathogenesis of idiopathic pulmonary fibrosis?

A

In IPF, the wound healing mechanisms become uncontrolled, leading to over-production of fibroblasts and deposition of increased extracellular matrix in the interstitium with little inflammation. The structural integrity of the lung parenchyma is therefore disrupted: there is loss of elasticity and the ability to perform gas exchange is impaired, leading to progressive respiratory failure.

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17
Q

What do respiratory function show in patients with IPF?

A

• Respiratory function tests usually show a restrictive pattern (FEV 1 /FVC ratio >70%) with reduced lung volumes and gas transfer. However, spirometry may be normal in early disease and lung volumes can be preserved in the presence of coexisting emphysema.

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18
Q

What appears on a chest X-ray in patients with IPF?

A

• Chest X-ray shows small-volume lungs with increased reticular shadowing at the bases but may be normal in early disease.

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19
Q

What does a high resolution CT show in patients with IPF?

A

Basal distribution : abnormalities are more pronounced at the bases.

Subpleural reticulation : reticulation is most evident in the lung peripheries.

Traction bronchiectasis : the fibrotic process distorts the normal lung architecture, pulling the airways open and causing bronchiectasis.

Honeycombing : there are basal layers of small, cystic airspaces with irregularly thickened walls composed of fibrous tissue.

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20
Q

What is the prognosis for patients with idiopathic pulmonary fibrosis?

A

The median survival time for patients with IPF is 2–5 years, although mortality is higher in the more acute forms.

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21
Q

What causes hypersensitivity pneumonitis?

A

Hypersensitivity pneumonitis (HP) is caused by an allergic reaction affecting the small airways and alveoli in response to an inhaled antigen or occasionally following ingestion of a causative drug.

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22
Q

What are the symptoms of hypersensitivity pneumonitis?

A

Symptoms include malaise, dyspnoea and cough. Weight loss is a prominent feature of subacute and chronic HP.

23
Q

What does auscultation of hypersensitivity pneumonitis show?

A

Auscultation reveals inspiratory squeaks due to bronchiolitis, and bilateral fine crackles.

24
Q

How do the inhaled antigens cause hypersensitivity pneumonitis?

A

Some of the inhalant materials may also lead to inflammation by directly activating the alternate complement pathway. These mechanisms attract and activate alveolar and interstitial macrophages so that continued antigenic exposure results in the progressive development of pulmonary fibrosis.

25
Q

Pneumonitis

A

Pneumonitis is a general term that refers to inflammation of lung tissue.

26
Q

Which antibody is involved in acute hypersensitivity? pneumonitis?

A

IgG

27
Q

What immune cells are involved in chronic hypersensitivity pneumonitis?

A

Chronic HP: CD4+ Th1 lymphocyte-mediated delayed hypersensitivity reaction
→ granuloma formation.

28
Q

How is hypersensitivity pneumonitis controlled?

A

Antigen avoidance

Steroids: for patients with severe disease, or those who fail to recover completely with antigen avoidance.

Immunosuppressive therapy: indicated in those with chronic disease that relapse or fail to come off steroids.

29
Q

Sarcoidosis

A

A multisystem disease of unknown aetiology characterised by tissue infiltration with non-caseating granulomas.

30
Q

What are the three key elements of diagnosing sarcoidosis?

A
  • Clinical + Radiological Compatibility
  • Exclusion of other diseases
  • Non-Caseating Granulomas (NCG)
31
Q

What is meant by non-caseating granulomas?

A

Non-necrotising

32
Q

What makes up sarcoid granulomas?

A
  • Central Core: tightly packed with macrophages, epithelioid cells, multinucleated giant cells, and CD4+ T lymphocytes.
  • Outer Area: mixture CD8 and CD4+ T lymphocytes, B lymphocytes, monocytes, mast cells, & fibroblasts, surrounded by lamellar rings of hyaline collagen.
33
Q

How do the sarcoid granulomas form?

A

Granuloma Formation: complex interplay of immune cells (e.g. macrophages, dendritic cells, T helper lymphocytes, T regulatory cells (Tregs)) and their mediators.

34
Q

What are the extrathoracic manifestations of sarcoidosis?

A

Eye, joints and skin.

35
Q

What is meant by granuloma, referring to sarcoidosis?

A

A granuloma is a mass or nodule composed of chronically inflamed tissue formed by the response of the mononuclear phagocyte system (macrophages/histiocytes).

36
Q

In what respiratory conditions are granulomas found?

A

Granulomas are seen in TB and other infections, including fungal and helminthic ones, in sarcoidosis and in hypersensitivity pneumonitis.

37
Q

What are the metabolic manifestations of sarcoidosis?

A

The metabolic manifestations are Hypercalcaemia and hypercalciuria can lead to the development of renal calculi, nephrocalcinosis and, ultimately, renal failure.

38
Q

Why does sarcoidosis cause hypercalcaemia?

A

Activated macrophages in lung and lymph nodes are able to hydroxylate vitamin D directly (independent of parathyroid hormone levels), leading to increased intestinal absorption of dietary calcium.

39
Q

How are bones and joints affected in sarcoidosis?

A

Bone and joint involvement . Arthralgia without erythema nodosum is seen in 5% of cases. Bone cysts with associated swelling, particularly affecting the digits, may be seen on X-ray.

40
Q

How are the eyes affected in sarcoidosis?

A

Eye lesions . Anterior uveitis is common and presents with misting of vision and a painful, red eye, but posterior uveitis may present simply as progressive loss of vision.

41
Q

How does IPF present on a CT and X-ray?

A

Marked reticular changes - fibrosis at the parenchyma.

Honeycomb change is a sign of advanced fibrosis.

Known as marked UIP.

42
Q

UIP

A

Usual interstitial pneumonia

43
Q

Usual interstitial pneumonia

A

Usual interstitial pneumonia (UIP) is a form of lung disease characterized by progressive scarring of both lungs.

Note: used interchangeably with IPF.

44
Q

What is meant by heterogeneity when referring to UIP?

A

You will find areas of normal lung interspersed with areas of abnormal lung.

45
Q

NSI

A

Non-specific interstitial pneumonia

46
Q

Non-specific interstitial pneumonia

A

A chronic IIP that is characterised by a homogeneous appearance of dense interstitial fibrosis with mild to moderate chronic interstitial inflammation.

47
Q

What is NSI commonly associated with?

A

Commonly associated with CTD (Scleroderma, Sjogren’s, myositis), drugs, HIV.

48
Q

IIP

A

Idiopathic interstitial pneumonia

49
Q

What distinguishes NSI from UIP?

A

UIP - has a heterogeneous appearance (areas of normal lung interspersed with areas of damaged lung.
IIP - has a homogeneous appearance of fibrosis throughout the lung.

50
Q

What is the general approach to interstitial lung disease care as a whole?

A 
ILD Specialist Nurse
Pulmonary Rehabilitation
O2 Assessment
Palliative Care
Dietitian
Psychology
Clinical Trials
Patient Support Groups
51
Q

What is the general treatment for IPF?

A

Anti-fibrotic therapy

52
Q

What is the general treatment for patients with interstitial lung disease that don’t have IPF?

A

Corticosteroids and Immunosuppressive therapy.

53
Q

What are the symptoms of asbestosis?

A

It is a progressive disease characterized by breathlessness and accompanied by finger clubbing and bilateral basal end-inspiratory crackles.

Respiratory 2 (22 decks)

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