Hypersensitivity Pneumonitis Final

8/3/2019 Hypersensitivity Pneumonitis Final

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Dr. Muhammad Amin


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Alternative Names

Extrinsic allergic alveolitis; Farmer's lung; Mushroom

picker's disease; Humidifier or air-conditioner lung; Bird

breeder's or bird fancier's lung

Hypersensitivity pneumonitis usually occurs in people who

work in places where there are high levels of organic dusts,

fungus, or molds.


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Bird fancier's lung is the most common type of HP. It is

caused by repeated or intense exposure to proteins found in

the feathers or droppings of many species of birds.

Farmer's lung is caused by exposure to dust from moldy

hay, straw, and grain.

These exposures can lead to lung inflammation and

acute lung disease. Over time, this acute condition may turn

into long-lasting (chronic) lung disease. HP is thought to be more common in non Smoker


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The term HP, is immunologically mediated, predominantly

interstitial lung diseases caused by inhalation of organic

dust related to occupational and environmental exposureantigen to which the individual has been previously

sensitized, primarily involves alveoli.


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These disorders account for about 15% of non infectious

diseases seen by pulmonary physician


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Bird fancier's lung

Also called bird breeder's lung,

pigeon breeder's lung, and poultry

worker's Lung.

Avian proteins Feathers and bird droppings[8]

Farmer's lung

The molds

Thermophilicactinomycetes[8]

Aspergillus species

Saccharopolyspora rectivirgula

,

and

Micropolyspora faeni

Moldy hay

Bagassosis Thermophilic actinomycetes[8]

Moldy bagasse (pressed

sugarcane)

Bird fancier's lung

Also called bird breeder's lung,

pigeon breeder's lung, and poultry

worker's Lung.

Avian proteins Feathers and bird droppings[8]

Farmer's lung

The molds

Thermophilicactinomycetes[8]

Aspergillus species

Saccharopolyspora rectivirgula

,

and

Micropolyspora faeni

Moldy hay

Bagassosis Thermophilic actinomycetes[8]

Moldy bagasse (pressed

sugarcane)


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Acute:

Influenza like symptoms begins 2-9 hours after exposure

Short period of exposure to high dose of antigen and

reversible. Peak typically 6-24hrs

Cough and dyspnea are common but not universal

Spontaneous resolve in 2-5 days

Recurrent symptoms when exposed to causative agents

Physical Examination => crackle


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Sub acute:

Gradual onset over several days to weeks

Marked dyspnea and cough may progress to severe

dyspnea and cyanosis leading to urgent hospitalization Mild symptoms

Extend over 10- 14 days

Usually reversible


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Chronic

Insidious onset over a period of month with increasing

cough and exertional dyspnea

Fatigue and weight loss may be prominent symptoms No fever

Chronic exposure to low antigen dose and is less reversal

able

Absence of clubbing of finger


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Immune complex mediated reaction

Cell mediated reaction=> granuloma formation


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Most patients have circulating immunoglobulin G antibodies

that are specific for the offending antigen. The antibody

(called precipitating antibody) reacts with a specific antigen

to form a precipitation.

Early response to the antigen is characterized by an

increase in neutrophils in the alveoli and small airways

followed by an influx of mononuclear cells. These cells

release proteolytic enzymes, prostaglandins, and

leukotrienes, play important roles in hypersensitivity

pneumonitis pathogenesis.


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Symptoms ofacute hypersensitivity pneumonitis may occur 4 -6 hours after you have left the area where the foreign substance isfound, making it difficult to find a connection between youractivity and the disease. Symptoms may include:

Chills

Cough

Fever Malaise

Shortness of breath


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Symptoms ofChronic Hypersensitivity Pneumonitis may

include:

Breathlessness, especially with activity

Cough, often dry

Loss of appetite

Unintentional weight loss


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Blood tests

Tests of molds from your workplace

Chest x-ray

HRCT scan of the chest

Lung function tests

Challenge test, in which you inhale the materials to which you are

sensitive to test your reaction

Lung biopsy


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Posteroanterior (PA) chest radiograph in a patient with chronic hypersensitivity

pneumonitis (HP)a pigeon fanciershows reticular-nodular opacification..


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Light microscopy shows mononuclear infiltration and noncaseating

granulomas. This finding is usually seen in acute disease, but it can also

appear in sub acute and chronic disease


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1. symptoms compatible with HP

2. evidence of exposure to appropriate antigen by history or

detection in serum and/or BAL fluid antibody

3. findings compatible with HP on chest radiograph or HRCT

4. BAL fluid lymphocytosis

5. pulmonary histologic changes compatible with HP

6. positive natural challenge


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1. Bibasilar rales

2. Decreased DLCO

3. Arterial hypoxemia, either at rest or during

exercise


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Asbestosis

A typical Pneumonias

Sarcoidosis Metastatic Cancer, Unknown Primary Site

Miliary Tuberculosis

Pneumonia, Viral

Drug induced Lung disease


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Contact avoidance exposure(job changing)

Environmental control

Changes in Industrial procedure Improve Ventilation

Air Mask ,Air Filtrating system

Drying of Hay prior to storage

Spraying of Bagasse with dilute propionic

acid


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Antipyretic & supplementary oxygen

Oral corticosteroids

20-50mg/day or 0.5 mg/kg/d for 2-4 weeks in

acute and maybe longer in sub acute and

chronic HP


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Highly variable

Is excellent following removal from antigen

exposure in Acute HP Recurrent episodes of acute HP do not

necessarily progress to chronic HP

Chronic HP may eventually lead to corPulmonale and death


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THANK YOU


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1. All of the following agents have been shown to cause both

occupational asthma and hypersensitivity pneumonitis EXCEPT:

A. Toluene diisocyanate

B. Trimellitic anhydride

C. Micropolyspora faeni

D. Bacillus subtilis

E. Diphenylmethane diisocyanate


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Which of the following groups of symptoms are common in

the chronic form of Hypersensitivity Pneumonitis?

A. Progressive dyspnea, cough, fever

B. Malaise, weakness, fever

C. Cough, malaise, anorexia

D. Cough, weakness, myalgias


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The immunologic basis of hypersensitivity pneumonitis

appears to be:

A. Type 3 (immune complex)

B. Type 1 (IgE)

C. Type 4 (Cell mediated)

D. Combination of Type 3 and Type 4

E. Combination of Type 1 and Type 3


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Which antigens are capable of inducing Hypersensitivity

Pneumonitis?

A. Bacteria, rodent products, plant products, and prions

B. Bacteria, viruses, low molecular weight chemicals,

and certain drugs

C. Fungi, amoebae, avian products, and certain drugs

D. Prions, viruses, bacteria, and fungi

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Hypersensitivity Pneumonitis Final