Extrinsic allergic alveoltis Flashcards

1
Q

Define extrinsic allergic aleveolitis.

A

AKA hypersensitivity pneumonitis

Result of non-IgE mediated immunological inflammation in alveoli and distal bronchioles, caused by repeated inhalation of non-human protein, e.g. natural plant or animal origin or a chemical conjugated to a human airway protein.

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2
Q

How do you classify hypersensitivity pneumonitis/EAA?

A

Acute (develops over hours following exposure)

Sub-acute (develops over weeks to months following exposure)

Chronic (develops over months to years following exposure).

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3
Q

What are the most common causative agents of EAA?

A

The most commonly reported agents are:

  • Bacteria (e.g., thermophilic Actinomycetes in farmer’s lung, bagassosis, and mushroom picker’s lung)
  • Animal proteins (e.g., avian proteins in pigeon breeder’s lung, bird fancier’s lung, and budgerigar fancier’s disease), + exposure to large farm animals
  • Fungi
  • Reactive chemicals such as acid anhydrides (epoxy resin lung disease), diisocyanates, and agents used in metal working are also known causes of HP syndrome
  • Ingested drugs
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4
Q

Which ingested drugs can cause HP?

A

nitrofurantoin, methotrexate, roxithromycin, and rituximab

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5
Q

Describe the pathophysiology of EAA.

A

Cellullar infiltrate consists of lymphocytes(CD3 CD8 CD4 Th1) plasma cells and neutrophils. Also presents with non-caseating granulomas and activated foamy macrophages. Broncho/bronchiolocentric inflammation and lymphocytic alveolitis

  • Acute HP - fever, tachypnoea, dyspnoea, pulmonary infiltrates, restrictive PFTs, reduced diffusing lung capacity of CO(DLCO) due to lymphocytic alveolitis.
  • Sub-acute HP - inflammation is not as intense and there is often a fair amount of fibrosis resulting in insidious development over many weeks of malaise, dyspnoea, cough, mixed PFTs and reduced DLCO.
  • Chronic HP - little inflammation, fibrosis characteristic of this type, results in dyspnoea,, weight loss, malaise, mixed PFTs and decreased DLCO.
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6
Q

What are the symptoms of extrinsic allergic alveolitis?

A
  • Dyspnoea
  • Non-productive/productive cough
  • Fever/chills
  • Malaise
  • Weight loss/anorexia
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7
Q

What would you find on examination of a patient with EAA?

A

Bibasilar or diffuse rales are usually present in people with sub-acute and chronic disease.

Approximately 50% of people with chronic HP have clubbing.

NB: rales are like sound of fire crackles, present on inspiration and expiration .

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8
Q

What are the risk factors for EAA?

A
  • Bird keeping and other hobbies
  • Regular use of hot tubs
  • Smoking
  • Viral infection
  • Specific occupations –>exposure to avian protein/mould/ bacterial /acid anhydride antigen or to metal-working fluid or diisocyanate (e.g.epoxy resin)
  • Oral intake of nitrofurantoin, methotrexate, roxithromycin, rituximab
  • Herbal supplements with ayurvedic medicine
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9
Q

Exposure to what accounts for about half of cases of HP?

A

Exposure to metal-working fluid

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10
Q

Why does smoking/viral infections predispose to HP?

A

Increases B7 co-stimulatory molecules on macrophages, thereby increasing the macrophage contribution to the inflammation.

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11
Q

List 3 types HP diseases caused by avian protein antigen.

A
  • Pigeon breeder’s lung
  • Bird fancier’s lung
  • Budgerigar fancier’s lung
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12
Q

Which bacterial/mould antigens can lead to HP?

A

Mould:

  • Aspergillus
  • Alternaria
  • Penicillium
  • Trichosporum

Bacterial:

  • Thermophilic Actinomycetes
  • Bacillus
  • Pseudomonas
  • Acinetobacter
  • Klebsiella
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13
Q

Descirbe the epidemiology of EAA.

A
  • 6-21% of pigeon breeders
  • Makes up less than 2% of all ILD cases
  • Prevalence of farmer’s lung in exposed farmers is about 0.5% and 3%
  • Can occasionally present in children
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14
Q

What investigations would you do for EAA?

A
  • Serology - for specific IgG
  • BAL - lymphocytosis
  • CXR
  • CT chest - upper/mid zone fibrosis
  • PFTs and diffusing lung capacity of CO - restrictive or mixed; decreased DLCO
  • FBC, ESR, albumin - check for leukocytosis, normocytic normochromic anaemia, elevated ESR, NO eosinophilia
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15
Q

What would you see on CXR/CT chest in EAA?

A

CXR - patchy, nodular infiltrates; fibrosis in chronic HP, may be normal between episodes. Generally CR is not v sensitive.

CT chest - shows ground-glass shadowing/multiple centrilobular ground glass nodules, mosaic attenuation, relative basal sparing.

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16
Q

What is the management of EAA?

A

Avoid precipitants, smoking cessation, pulmonary rehabilitation, supplemental oxygen (at _<_89%)

Oral corticosteroids - may need to be long term but start with 1mg/kg/day then taper with alternate day therapy for 6 weeks

17
Q

What are the complications and prognosis of EAA?

A

Patients with non-fibrotic disease and allergen avoidance have good prognosis. Any fibrosis is unlikely to normalise.

  • Progressive deterioration
  • Hypoxaemia
  • Death - due to lung destruction