B Industrial Bronchitis in Objective-C

Generation Denso QR Bar Code in Objective-C B Industrial Bronchitis

Industrial bronchitis is chronic bronchitis found in coal miners and others exposed to cotton, flax, or hemp dust Chronic disability from industrial bronchitis is infrequent

Byssinosis is an asthma-like disorder in textile workers caused by inhalation of cotton dust The pathogenesis is obscure Chest tightness, cough, and dyspnea are characteristically worse on Mondays or the first day back at work,

Mapp CE et al Occupational asthma Am J Respir Crit Care Med 2005 Aug 1;172(3):280 305 [PMID: 15860754] Singh N et al Review: occupational and environmental lung disease Curr Opin Pulm Med 2002 Mar;8(2):117 25 [PMID: 11845007]

Asthma -Blockers Aspirin Nonsteroidal anti-inflammatory drugs Histamine Methacholine Acetylcysteine Aerosolized pentamidine Any nebulized medication Chronic cough Angiotensin-converting enzyme inhibitors Pulmonary infiltration Without eosinophilia Amitriptyline Azathioprine Amiodarone With eosinophilia Sulfonamides

Pulmonary edema Noncardiogenic Aspirin Chlordiazepoxide Cocaine Ethchlorvynol Heroin Cardiogenic -Blockers Pleural effusion Bromocriptine Nitrofurantoin Any drug inducing systemic lupus erythematosus Methysergide Chemotherapeutic agents Mediastinal widening Phenytoin Corticosteroids Methotrexate Respiratory failure Neuromuscular blockade Aminoglycosides Succinylcholine Gallamine Dimethyltubocurarine (metocurine) Central nervous system depression Sedatives Hypnotics Opioids Alcohol Tricyclic antidepressants Oxygen

Typical patterns of pulmonary response to drugs implicated in drug-induced respiratory disease are summarized in Table 9 26 Pulmonary injury due to drugs occurs as a result of allergic reactions, idiosyncratic reactions, overdose, or undesirable side effects In most patients, the mechanism of pulmonary injury is unknown Precise diagnosis of drug-induced pulmonary disease is often difficult, because results of routine laboratory studies are not helpful and radiographic findings are not specific A high index of suspicion and a thorough medical history of drug usage are critical to establishing the diagnosis of drug-induced lung disease The clinical response to cessation of the suspected offending agent is also helpful Acute episodes of drug-induced pulmonary disease usually disappear 24 48 hours after the drug has been discontinued, but chronic syndromes may take longer to resolve Challenge tests to confirm the diagnosis are risky and rarely performed Treatment of drug-induced lung disease consists of discontinuing the offending agent immediately and managing the pulmonary symptoms appropriately Inhalation of crack cocaine may cause a spectrum of acute pulmonary syndromes, including pulmonary infiltration with eosinophilia, pneumothorax and pneumomediastinum, bronchiolitis obliterans, and acute respiratory failure associated with diffuse alveolar damage and alveolar hemorrhage Corticosteroids have been used with variable success to treat alveolar hemorrhage

Babu KS et al Drug-induced airway diseases Clin Chest Med 2004 Mar;25(1):113 22 [PMID: 15062603] Huggins JT et al Drug-induced pleural disease Clin Chest Med 2004 Mar;25(1):141 53 [PMID: 15062606]

Nitrofurantoin Penicillin Methotrexate Crack cocaine Drug-induced systemic lupus erythematosus Hydralazine Procainamide Isoniazid Chlorpromazine Phenytoin Interstitial pneumonitis/ fibrosis Nitrofurantoin Bleomycin Busulfan Cyclophosphamide Methysergide Phenytoin

The lung is an exquisitely radiosensitive organ that can be damaged by external beam radiation therapy The degree of pulmonary injury is determined by the volume of lung irradiated, the dose and rate of exposure, and potentiating factors (eg, concurrent chemotherapy, previous radiation therapy in the same area, and simultaneous withdrawal of corticosteroid therapy) Symptomatic radiation lung injury occurs in about 10% of patients treated for carcinoma of the breast, 5 15% of patients treated for carcinoma of the lung, and 5 35% of patients treated for lymphoma Two phases of the pulmonary response to radiation are apparent: an acute phase (radiation pneumonitis) and a chronic phase (radiation fibrosis)

Radiation pneumonitis usually occurs 2 3 months (range 1 6 months) after completion of radiotherapy and is characterized

by insidious onset of dyspnea, intractable dry cough, chest fullness or pain, weakness, and fever The pathogenesis of acute radiation pneumonitis is unknown, but there is speculation that hypersensitivity mechanisms are involved The dominant histopathologic findings are a lymphocytic interstitial pneumonitis progressing to an exudative alveolitis Inspira-