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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