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Internal Medicine > Harrison - Hypersensitivity Pneumonitis and Pulmonary Infiltrates with Eosinophilia > Flashcards

Harrison - Hypersensitivity Pneumonitis and Pulmonary Infiltrates with Eosinophilia Flashcards

1
Q

What is HP?

A

Extrinsic allergic alveolitis - An inflammatory disorder of the lung involving alveolar walls and terminal airways that is induced by repeated inhalation of a variety of organic agents in a susceptible host.

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2
Q

In the US, what are the 3 MC types of HP?

A
  1. Farmer’s lung.
  2. Bird fancier’s lung.
  3. Chemical worker’s lung.
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3
Q

Farmer’s lung - Cause?

A

Inhalation of proteins, such as thermophilic bacteria and fungal spores that are present in moldy bedding and feed.

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4
Q

The antigens responsible for farmer’s lung are also responsible for?

A
  1. Mushroom worker’s disease - moldy composted growth medium.
  2. Bagassosis - moldy sugar cane.
  3. Water-related exposure - molds in air conditioners or humidifiers.
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5
Q

Hot tub lung?

A

Hypersensitivity reaction to Mycobacterium avium complex, which is present in hot tubs or whirlpools and is differentiated from actual infection.

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6
Q

Interestingly, what is the effect of smoking in HP?

A

Has been associated with DECREASED incidence of HP - HOWEVER, smoking may lead to a more progressive or severe course of HP once the disease is present.

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7
Q

Pathogenesis of HP - What characterizes the very early (acute) reaction?

A

An increase in PMNs in the alveoli and small airways.

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8
Q

Pathogenesis of HP - What does studies in animal models suggest?

A

That the disease is a Th1-mediated immune response to antigen, with IFN-gamma, IL-12, and possibly IL-18 contributing to disease expression - Multiple cytokines interact to promote HP.

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9
Q

Is there a genetic predisposition to the development of HP?

A

Certain polymorphisms of the TNF-alpha promoter region and major histocompatibility complex reportedly confer an enhanced susceptibility to pigeon breeder’s disease.

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10
Q

After inhalation of an antigenic particle, the attraction and accumulation of inflammatory cells in the lung may be due to one or more of the following mechanisms?

A
  1. Induction of the adhesion molecules L-selectin and E-selectin.
  2. Elaboration by dendritic cells of CC chemokine 1 (DC-CK-1/CCL18).
  3. Increased expression of CXCR3/CXCL10 by CD4+ and CD8+ lymphocytes.
  4. Incr. levels of Fas protein and FasL in the lung (which would be expected to suppress inflammation by induction of T cell apoptosis) is COUNTERBALANCED by increased expression of the inducible anti-apoptotic gene Bcl-xL –> Lower overall level of pulmonary lymphocyte apoptosis in HP patients.
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11
Q

Clinical presentation of HP?

A

That of an interstitial pneumonitis - Can be acute, subacute, and chronic.

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12
Q

Acute HP - Clinical presentation?

A 
6-8h after exposure:
1. Cough.
2. Dyspnea.
3. Fever/Chills.
4. Malaise.
usually clear within a few days if there is no further exposure to antigen.
Resembles influenza.
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13
Q

Subacute HP - Clinical presentation?

A

Often appears insidiously over a period of weeks marked by cough and dyspnea - May progress to cyanosis and severe dyspnea, requiring hospitalization.

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14
Q

Chronic HP - Clinical presentation?

A

May be indistinguishable from pulmonary fibrosis in its later stages.

  1. Cough.
  2. Weight loss.
  3. Malaise.
  4. Gradual increase in dyspnea.
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15
Q

Chronic HP - Physical exam may reveal?

A
  1. Clubbing.

2. Inspiratory crackles.

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16
Q

Chronic HP - Imaging shows?

A
  1. Interstitial fibrosis.

2. Emphysema.

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17
Q

What is the clinical manifestation of chronic HP with the greatest predictive value for mortality?

A

Pulmonary fibrosis.

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18
Q

Fibrosis appears more prominent in HP associated with?

A

Birds.

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19
Q

Emphysema appears more prominent in HP associated with?

A

Farmer’s lung.

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20
Q

Antigen for bird fancier’s, breeder’s, or handler’s lung?

A

Parakeet, pigeon, chicken, turkey proteins from avian droppings or feathers.

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21
Q

Antigen for chemical worker’s lung?

A

Isocyanates from polyurethane foam, varnishes, lacquer.

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22
Q

Antigen for farmer’s lung?

A

Thermophilic actinomycetes from “Moldy” hay, grain, silage.

23
Q

All forms of HP may be associated with INCREASED?

A
  1. ESR.
  2. CRP.
  3. RF.
  4. LDH.
  5. Serum Ig.
24
Q

What blood changes do we see in HP?

A
  1. Neutrophilia.
  2. LymphoPENIA.
  3. NO EOSINOPHILIA.
25
Q

The occurrence of precipitins indicates what regarding HP?

A

Sufficient exposure to the causative agent for generation of an immunologic response and is one of the major diagnostic criteria.

26
Q

CXR in HP?

A

No specific or distinctive features - May be normal even in symptomatic patients.

27
Q

Acute/Subacute phases may be associated with what?

A
  1. Poorly defined, patchy, or diffuse infiltrates.
  2. Discrete, nodular infiltrates.
  3. Air-space consolidation.
28
Q

Chronic HP may show in CXR?

A
  1. Usually shows diffuse reticulonodular infiltrate.
  2. Honeycombing may eventually develop as the condition progresses.
  3. Apical sparing is common –> Disease severity correlates with inhaled antigen load, but no particular distribution or pattern is classic for HP.
29
Q

What has become the procedure of choice for imaging HP?

A

High-resolution CT.

30
Q

Pulmonary function studies in all forms of HP may show?

A

A restrictive OR an obstructive pattern with loss of:

  1. Lung volumes.
  2. Impaired diffusing capacity.
  3. Decr. compliance.
  4. Resting or exercise-induced hypoxemia may be seen.
  5. Bronchospasm and bronchial hyperreactivity are sometimes found in acute HP.
31
Q

What is the role of bronchoalveolar lavage in HP?

A

In some centers for diagnostic evaluation.

  1. Marked lymphocytic alveolitis on BAL in almost universal (not pathognomonic).
  2. Lymphocytes show DECREASED helper/suppressor ration, although this ration can be variable –> depending on the dose and duration of exposure.
  3. Alveolar neutrophilia is also prominent ACUTELY.
  4. Mastocytosis may correlate with disease activity.
32
Q

Role of lung biopsy in HP?

A

May be diagnostic - The histopathology is distinctive, although NOT pathognomonic of HP.

33
Q

Active phase of HP - Histopathology?

A
  1. Interstitial alveolar infiltrate with plasma cells, lymphocytes, and occasional eosinophils and neutrophils, usually accompanied by loose, non caseating peribronchial granulomas.
  2. Some degree of bronchiolitis in about 50% of cases.
  3. Rarely, bronchiolitis obliterans with organizing pneumonia (BOOP).
34
Q

Subacute phase of HP - Histopathology?

A

Triad of:

  1. Mononuclear bronchiolitis.
  2. Interstitial infiltrates of lymphocytes and plasma cells.
  3. Non necrotizing, randomly scattered parenchymal granulomas without mural vascular involvement is CONSISTENT with HP.
    - -> Interstitial fibrosis may be present, but it is often mild in earlier stages of the disease.
35
Q

Chronic HP - Histopathology?

A
  1. Variable pathology and may resemble non specific interstitial pneumonia, organizing pneumonia, or usual interstitial pneumonia. Granulomas may or may NOT be present.
  2. Centrilobular fibrosis.
  3. Peribronchial inflammation with fibrosis.
  4. Bridging fibrosis, and emphysema are common.
36
Q

A prediction rule for the clinical diagnosis of HP has been developed by the International HP Study Group. Six significant predictors of HP?

A
  1. Exposure to a known antigen.
  2. Positive predictive antibodies to the antigen.
  3. Recurrent episodes of symptoms.
  4. Inspiratory crackles.
  5. Symptoms developing 6-8h after exposure.
  6. Weight loss.
37
Q

It is clear that the diagnosis of HP is established by?

A
  1. Consistent symptoms, physical findings, pulmonary function tests, and radiographic tests.
  2. A history of exposure to a recognized antigen.
  3. Identification of an antibody to that antigen (ideally).
38
Q

What is the most important tool in diagnosing HP?

A

A high index of suspicion.

39
Q

The DDX for HP involves?

A
  1. Drug-induced lung disease.
  2. Collagen vascular disorder.
  3. Sarcoidosis.
  4. Allergic bronchopulmonary mycoses.
  5. Eosinophilic pneumonias.
40
Q

Treatment of patients with acute HP?

A

Usually recover without need for glucocorticoids.

41
Q

Treatment for patients with subacute HP?

A

Urgent establishment of the diagnosis and prompt institution of glucocorticoids treatment are indicated in such patients.
–> Prednisone at a dosage of 1mg/kg per d or its equivalent is continued for 7 to 14 days and then tapered over the ensuing 2-6wks at a rate that depends on the patient’s clinical status.

42
Q

Treatment of patients with chronic HP?

A

May gradually recover WITHOUT therapy, following environmental control.

  • -> In many, a trial of prednisone may be useful to obtain maximal reversibility of the lung disease.
  • -> 1mg/kg/d for 2-4wks - then taper to the lowest dosage that will maintain the functional status of the patient.
43
Q

Pulmonary infiltrates with eosinophilia (PIE) or eosinophilic pneumonias - Etiology known?

A
  1. Allergic bronchopulmonary mycoses.
  2. Parasitic infestations.
  3. Drug reactions.
  4. Eosinophilia-myalgia syndrome.
44
Q

PIE or eosinophilic pneumonias - Idiopathic?

A
  1. Loeffler’s syndrome.
  2. Acute eosinophilic pneumonia.
  3. Chronic eosinophilic pneumonia.
  4. Allergic granulomatosis of Churg-Strauss.
  5. Hypereosinophilic syndrome.
45
Q

What is the main difference between PIE and HP?

A

May be considered as immunologically mediated lung diseases - but are NOT to be confused with HP, in which eosinophilia is NOT a feature.

46
Q

What should be suspected when an eosinophilic pneumonia is associated with bronchial asthma?

A

Important to determine if the patient has atopic asthma and has a wheal-and-flare skin reactivity to Aspergillus or other relevant fungal antigens –> Criteria for ABPA.

47
Q

Main diagnostic criteria for ABPA?

A
  1. Bronchial asthma.
  2. Pulmonary infiltrates.
  3. Peripheral eosinophilia (>1.000/μL).
  4. Immediate wheal-and-flare response to Aspergillus fumigatus.
  5. Serum precipitins to A.fumigatus.
  6. Elevated serum IgE.
  7. CENTRAL bronchiectasis.
48
Q

Other diagnostic features for ABPA?

A
  1. History of brownish plugs in sputum.
  2. Culture of A.fumigatus from sputum.
  3. Elevated IgE (and IgG) class antibodies specific for A.fumigatus.
49
Q

The bronchial asthma of ABPA likely involves an?

A

IgE-mediated hypersensitivity.

50
Q

The bronchiectasis associated with ABPA is thought to result from?

A

Deposition of immune complexes in proximal airways.

51
Q

Treatment of ABPA?

A

Long term use of corticosteroids.

52
Q

Besides ABPA, another eosinophilic process associated with asthma?

A

Churg-Strauss syndrome –> necrotizing eosinophilic vasculitis and eosinophilic infiltration or multiple organs, including the lung.

53
Q

Hypersensitivity pneumonitis (HP) was first described in?

A

1874.

Internal Medicine (107 decks)

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