hypersense pneumo

8/7/2019 hypersense pneumo

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:

Hypersensitivity Pneumonitis

Definition :

Hypersensitivity Pneumonitis

- foreign substance

n mm antigen

-mn antibody m-n

Pathogenesis :

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. However, approximately 50% of asymptomatic

persons exposed to the sensitizing antigen also have these

antibodies.


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Areas of organizing pneumonia

http://www.flickr.com/photos/pulmonary_pathology/5172311003

/in/photostream/

Acute hypersensitivitypneumonitis: Little is known about the

gross pathologic features of acute hypersensitivity

pneumonitis. The pathologic features of acute hypersensitivity

pneumonitis in farmerts lung include a neutrophil and

eosinophil infiltration of the alveolar spaces, vessel vasculitis,

and in some cases, diffuse alveolar damage. Addi ionally,

immunopa hologic s udies have revealed immunoglobulin and

complemen deposi ion in he vessels.

Subacute hypersensitivitypneumonitis: The his opa hologics

fea ures of subacu e hypersensi ivi y pneumoni is comprise a


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Interstitial inflammation associated with fibrosis. Chronic

hypersensitivitypneumonitis

http://emedicine.medscape.com/article/299174diagnosis


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Granulomatous vasculitis. mononuclear infiltration and

noncaseating granulomas usually observed in association with

acute hypersensitivitypneumonitis,http://www.flickr.com/photos/pulmonary_pathology/5172311391

/in/photostream/

granulomatous interstitial pneumonia, diffuse its features, but

nonspecific. Along the airway and thickening of the alveolar

septum in the infiltration of lymphocytes and plasma cells.

Nonnecrotizing granulomas, scattered in the lung

parenchyma, not involving the vessel wall, fibrosis often minor,

and disease staging.


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.

Thickening of the alveolar septum in the infiltration of

lymphocytes and plasma cells. Non-necrotizing granulomas,

scattered in the lung parenchyma, not involving the vessel

wall, fibrosis often minor, and disease staging.http://www.healthwritings.com/withhypersensitivity

pneumonitis/


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Clinical Manifestation :

Hypersensitivity pneumonitis has been divided into 3 forms of

diseases depending on the length of time of exposure. Note

the following:

y Acute hypersensitivitypneumonitis is due to a brief butintermittent intense exposure to an offending agent.

Symptoms begin 48 hours after exposure and resemble

the flu. Features include cough, dyspnea, fever, malaise,

diaphoresis, headaches, and myalgias. Chest

radiography shows an interstitial pattern, and HRCT

demonstrates groundglass opacities. Symptoms resolve

in 1224 hours, and the patient returns to his or hernormal baseline state. If exposure is controlled, longterm

sequelae are limited.

y Subacute hypersensitivitypneumonitis is due to a lowlevel but prolonged exposure to an inciting agent.

Symptoms resemble those of chronic bronchitis andinclude chronic cough, exertional dyspnea, malaise,

anorexia, fatigue, and weight loss. Chest radiography

shows a reticulonodular pattern in midtoupper lung


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fields. HRCT reveals micronodules, groundglass

opacities, and early fibrosis. With recognition and

avoidance of the antigen, patients may have complete

recovery. With continued exposure, however, more than

half the patients progress to endstage lung disease.

y Chronic hypersensitivitypneumonitis is the finaldestination from uncontrolled acute or subacute disease.

Signs and symptoms resemble those of endstage

interstitial pulmonary fibrosis. Radiographic findingsinclude fibrosis and honeycombing. Prognosis is poor,

with continued deterioration of lung function.

Bilateral reticulonodular densities chronic hypersensitivity

pnemonitis

http://imaging.consult.com/imageSearch?query=conventional&t

hes=true&resultOffset=4200


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bilateral reticulonodular interstitial infiltration secondary tosubacute hypersensitivitypneumonitis.

http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijrh

/vol4n2/pneumonitis.xml

In acute hypersensitivity pneumonitis, a diffuse micronodular

interstitial pattern (at times with groundglass density in the

lower and middle lung zones) may be observed. Findings are

normal in approximately 10% of patients.

In subacute hypersensitivity pneumonitis, micronodular or

reticular opacities are most prominent in midtoupper lung

zones.


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In chronic hypersensitivity pneumonitis, progressive fibrotic

changes with loss of lung volume particularly affect the upper

lobes. Nodular or groundglass opacities are not present.

Features ofemphysema are found on significant chest films

and CT scans. Note the image below:

http://emedicine.medscape.com/article/299174diagnosis

Diagnosis :

The following 6 clinical predictors can be used to help

establish hypersensitivity pneumonitis as the correct diagnosis:

y Exposure to a known offending antigeny Positive precipitating antibodies to the offending antigeny

Recurrent episodes of symptomsy Inspiratory crackles on physical examinationy Symptoms occurring 48 hours after exposurey Weight loss


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Based on these criteria, the diagnosis of hypersensitivity

pneumonitis can often be made or rejected with confidence,

especially in areas of high or low prevalence, respectively,without bronchoalveolar lavage (BAL) or biopsy

Blood tests are of limited utility. Leukocytosis and neutrophilia,

elevated erythrocyte sedimentation rate, and increased levels

of quantitative immunoglobulins and Creactive protein are

observed in many patients. Precipitating immunoglobulin G

antibodies against potential antigens indicate prior exposure

and sensitization but do not necessarily represent disease.

Many patients with clinical disease have no detectableantibodies, owing either to testing with an inappropriate

antibody or to cessation of exposure.

Treatment :1.Antigen avoidance2.Corticosteroid therapy


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3.Prednisone (Sterapred) chronic hypersensitivitypneumonitis

http://emedicine.medscape.com/article/299174treatment

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