Emphysema pulmonary

Emphysema, pulmonary The swelling and breaking down of the air sacs in the lungs. This reduces the area available for oxygen and carbon dioxide exchange within the lungs. 

Acute and chronic bronchitis, pneumonia, upper respiratory infection, pulmonary emphysema, pulmonary heart disease, heart failure, acute nephritis and renal failure, chronic nephritis, gastritis, hypothyroidism, hypoadrenalism, fibromyalgia, rheumatic arthritis and rheumatoid arthritis. 

Acute and chronic bronchitis, asthma, emphysema, pulmonary heart disease, heart failure. 

Respiratory aspects dyspnea from absorption of metal dust or fume, emphysema, pulmonary fibrosis, formation of granuloma, chronic asthma. 

HUMAN HEALTH RISKS Inhalation human LCLo 500 ppm for 5 minutes Acute Risks changes in trachea or bronchi emphysema pulmonary edema or congestion irritation of eyes, mucous membranes liquid bums skin Chronic Risks minor changes in pulmonary function. 

Despite case reports of response to treatment with corticosteroids, larger studies have not shown any outcome benefit. Currently, accepted treatment options are limited to supportive care and prevention and treatment of infection. There is a report of three BMT recipients with IPS whose lung function improved following etanercept administration (13). Lung transplant may offer a therapeutic option for selected patients. Although the pneumonitis resolves in about 31%, the clinical course of IPS is often comphcated by viral and fungal infections, pneumothorax, pneumomediastinum, subcutaneous emphysema, pulmonary fibrosis, and autoimmune polyserositis (5). The case fatality of IPS is... 

Epidemiological studies of nickel-producing and nickel-using workers seldom indicate excess mortaUty from nonmalignant respiratory disease. Evidence for such effects exists mainly as a few reports of isolated incidents of asthma, pulmonary fibrosis, chronic bronchitis, and emphysema in nickel workers. Nickel may or may not play a causal role in these incidents (131). 

Chronic Pulmonary Toxicity Chronic damage to the lungs may be due to several subsequent exposures or due to one large dose that markedly exceeds the capacity of pulmonary defense, clearance, and repair mechanisms. Chronic pulmonary toxicity includes emphysema, chronic bronchitis, asthma, lung fibrosis, and lung cancer. The single most important reason for chronic pulmonary toxicity is tobacco smoke, which induces all types of chronic pulmonary toxicity, with the exception of fibrosis. 

The definition above has replaced older ones that focused to varying degrees on chronic bronchitis and/ or emphysema. Chronic bronchitis and emphysema frequently represent different consequences of the same insult leading to changes in large aiiways, small airways and pulmonary parenchyma (Table 1). 

Other disorders of the lower respiratory tract include emphysema (lung disorder in which the terminal bronchioles or alveoli become enlarged and plugged with mucus) and chronic bronchitis (chronic inflammation and possibly infection of die bronchi). Chronic obstructive pulmonary disease (COPD) is die name given collectively to emphysema and chronic bronchitis because die obstruction to die airflow is present most of the time. Asdima diat is persistent and present for most of die time may also be referred to as COPD. 

Sympathomimetics (drugs that mimic the sympathetic nervous system) are used primarily to treat reversible airway obstruction caused by bronchospasm associated with acute and chronic bronchial asthma, exercise-induced bronchospasm, bronchitis, emphysema, bronchiectasis (abnormal condition of the bronchial tree), or other obstructive pulmonary diseases. 

During tiie ongoing assessment, tiie nurse assesses the respiratory status every 4 hours and whenever tiie drug is administered. The nurse notes the respiratory rate, lung sounds, and use of accessory muscles in breathing, hi addition, tiie nurse keeps a careful record of the intake and output and reports any imbalance, which may indicate a fluid overload or excessive diuresis. It is important to monitor any patient with a history of cardiovascular problems for chest pain and changes in the electrocardiogram. The primary health care provider may order periodic pulmonary function tests, particularly for patients with emphysema or bronchitis, to help monitor respiratory status. 

In the past number of years a number of studies have shown that in a variety of diseases there is a significant oxidation of Met residues to Met(O) in specific proteins that results in a loss of biological activity. These diseases include cataracts, rheumatoid arthritis, adult respiratory distress syndrome and emphysema. The most convincing evidence that Met(O) in proteins may be involved in the etiology of a pathological condition comes from studies with a-l-PI. It is well accepted that a-l-PI is inactivated upon oxidation of its Met residues. A decreased activity of a-l-PI in lung tissue that would result in an increased elastase activity has been associated with pulmonary emphysema. In patients who have a... 

J. Bignon and G. L. Scarpa (Eds.), Biochemistry, Pathology and Genetics of Pulmonary Emphysema Proceedings of a Meeting held at Porto Conte, Sassari, April 27-30, 1981, Pergamon, New York, 1981. 

Deletions in the elastin gene (located at 7qll.23) have been found in approximately 90% of subjects with Williams syndrome, a developmental disorder affecting connective tissue and the central nervous system. The mutations, by affecting synthesis of elastin, probably play a causative role in the supravalvular aortic stenosis often found in this condition. A number of skin diseases (eg, scleroderma) are associated with accumulation of elastin. Fragmentation or, alternatively, a decrease of elastin is found in conditions such as pulmonary emphysema, cutis laxa, and aging of the skin. 

Mauderly, J.L. (1984). Respiratory function responses of animals and man to oxidant gases and to pulmonary emphysema. J. Toxicol. Environ. Health 13, 345-361. 

Phagocyte-derived ROMs have been implicated in the pathogenesis of a number of pulmonary diseases, including emphysema, acute respiratory distress syndrome, and various environmental diseases such as asbestos-related fibrosis and cancer (Mossman and Marsh, 1985). The relatively high oxygen tension in pulmonary tissue renders the lung prone to oxidative stress (Edwards and Lloyd, 1988). 

Mineral dust-induced ROMs contributes to pulmonary fibrosis, malignancy, hypersensitivity and emphysema (Doelman etctl., 1990 Kamp etui., 1992). The involvement of ROMs in pulmonary fibrotic reactions is indicated by the participation of PMN oxidants in the autoactivation of latent coUagenase (Weiss et al., 1985). Prolyl hydroxylase, a key enzyme in collagen fibril formation, has been shown to be dependent on the reaction of superoxide with prolyl residues (Myllyla et al., 1979). 

A substance known as elastase is involved in various inflammatory diseases such as arthritis, pulmonary emphysema, and pancreatitis. Elastase activity can be inhibited by a compound known as elasnin, obtained from a microorganism. 

Human leukocyte elastase is a protease that degrades elastin and other connective tissue components. It is implicated in the pathogenesis of pulmonary emphysema and other inflammatory diseases such as rheumatoid arthritis and cystic fibrosis. Porcine pancreatic elastase has often been used as a model for HLE. Both enzymes have a small primary binding site Si. 

---