Obstructive respiratory diseases

An essential importance for the development of obstructive respiratory diseases, within the scope of cancer mortality of smokers, was indicated by epidemiological studies. It was shown that the relative risk for smokers, with obstructive ventilation parameters [FEV 1% < 60 (Melv)m et al., 1987), respectively 70] (Skillud et al., 1987), to be affected by lung cancer, is significantly higher than that of comparative groups with normal lung-function parameters. 

A survey about the dietary habits within the scope of the "National Health and Nutritional Examination Survey" showed that an inverse correlation (Morabia et al., 1989) exists between COPD and vitamin A supply as the only one of 12 examined dietary components. If a diminished supply of vitamin A increases the appearance of obstructive respiratory diseases, a marginal or local vitamin A deficit could be responsible for the observed changes of the respiratory mucosa. Such a deficit results in a loss of cilia, an increase of secreting cells and finally the formation of squamous metaplasia (Biesalski et al., 1985 Chytil, 1985 Shah and Rajalekshmi, 1984). 

Chronic obstructive respiratory disease ai-antitrypsin deficiency Mucoviscidosis Sarcoidosis... 

Primary pulmonary diseases (e.g. primary pulmonary hypertension, pulmonary fibrosis, chronic obstructive respiratory diseases) cause chronic hepatic congestion due to chronic pulmonary heart disease, possibly leading to insufficiency. Hypoxaemia as a result of acute or chronic respiratory insufficiency can impair metabolic liver functions considerably. In 40—70% of patients with cirrhosis, hypoxaemia can be found in about 50% of cases with advanced cirrhosis, a reduced diffusion capacity for CO is detectable. Furthermore, pulmonary tissue contains a high level of glutamine synthetase, so that ammonia detoxification is possible (ultimately by perivenous hepatocytes) before the blood reaches the systemic circulation. In existing pulmonary diseases, localized ammonia detoxification is impaired. 

Waal-Manning HJ, Simpson FO. Safety of celiprolol in hypertensives with chronic obstructive respiratory disease. NZ Med J 1990 103 222. 

Halken S, Host A, Nilsson L, Taudorf E Passive smoking as a risk factor for development of obstructive respiratory disease and allergic sensitization. Allergy 1995 50 97—105. (IV)... 

COPD, chronic obstructive pulmonary disease EAE, experimental autoimmune encephalomyelitis RSV, respiratory syncytial virus SLE, systemic lupus erythematosus. 

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. 

A 67-year-old man with a history of chronic obstructive pulmonary disease presents to the emergency department with high fevers, shaking chills, severe chest pain, and shortness of breath. His family members state that he has been confused all day. He started having a severe cough 2 days ago, with excessive sputum production. He received doxycycline 100 mg twice daily for an upper respiratory tract infection 7 days ago. 

Respiratory acidosis Acidosis caused by retention of carbon dioxide due to a respiratory abnormality (e.g., chronic obstructive lung disease). 

Infection of the trachea and bronchi causes hyperemic and edematous mucous membranes and an increase in bronchial secretions. Destruction of respiratory epithelium can range from mild to extensive and may affect bronchial mucociliary function. In addition, the increase in bronchial secretions, which can become thick and tenacious, further impairs mucociliary activity. Recurrent acute respiratory infections may be associated with increased airway hyperreactivity and possibly the pathogenesis of chronic obstructive lung disease. 

In a patient with chronic respiratory acidosis (e.g., chronic obstructive pulmonary disease), treatment is essentially similar to that for acute respiratory acidosis with a few important exceptions. Oxygen therapy should be initiated carefully and only if the Pao2 is less than 50 mm Hg because the drive to breathe depends on hypoxemia rather than hypercarbia. 

Metabolic alkalosis and respiratory acidosis can occur in patients with chronic obstructive pulmonary disease and respiratory acidosis who are treated with salt restriction, diuretics, and possibly glucocorticoids. 

DIAGNOSIS OF ACUTE RESPIRATORY FAILURE IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE ... 

The AEGL-1 concentration was based on a 1-hour (h) no-effect concentration of 8,000 parts per million (ppm) in healthy human subjects (Emmen et al. 2000). This concentration was without effects on pulmonary function, respiratory parameters, the eyes (irritation), or the cardiovascular system. Because this concentration is considerably below that causing any adverse effect in animal studies, an intraspecies uncertainty factor (UF) of 1 was applied. The intraspecies UF of 1 is supported by the absence of adverse effects in therapy tests with patients with severe chronic obstructive pulmonary disease and adult and pediatric asthmatics who were tested with metered-dose inhalers containing HFC-134a as the propellant. Because blood concentrations in this study approached equilibrium following 55 minutes (min) of exposure and effects are determined by blood concentrations, the value of 8,000 ppm was made equivalent across all time periods. The AEGL-1 of 8,000 ppm is supported by the absence of adverse effects in experimental animals that inhaled considerably higher concentrations. No adverse effects were observed in rats exposed at 81,000 ppm for 4 h (Silber and Kennedy 1979) or in rats exposed... 

Aerosolised medicines have been used for centuries to treat respiratory diseases, with inhalation therapy for the airways focused primarily on the treatment of asthma and chronic obstructive pulmonary disease (COPD). The development of new products for delivery to the lungs for these respiratory diseases includes new steroids and beta agonists plus combination products featuring both agents. New classes of anti-asthma medication are also being developed for inhalation with the aim of delivering them directly to the inflamed airways. 

Diazepam can cause central nervous system depression. It may cause respiratory depression in overdosage but, at hypnotic doses, the risk of hyperventilation in patients with severe chronic obstructive pulmonary disease is minimal. 

Chronic obstructive pulmonary disease Lower respiratory infections... 

Some studies of survivors of massive chlorine exposures have shown either persistent obstructive or restrictive deficits, but pre-exposure data on these patients were not available. Persistent respiratory symptoms, bronchial obstruction, and bronchial hyperresponsiveness were observed in 82%, 23%, and 41 % of chronically exposed pulp mill workers, respectively, 18-24 months after cessation of exposure." In most cases it is not known whether prolonged symptoms after chlorine exposure are due to aggravation of preexisting conditions such as tuberculosis, asthma, chronic obstructive pulmonary disease, or heart disease." "... 

Particulate matter air pollution is especially harmful to people with lung disease such as asthma and chronic obstructive pulmonary disease (COPD), which includes chronic bronchitis and emphysema, as well as people with heart disease. Exposure to particulate air pollution can trigger asthma attacks and cause wheezing, coughing, and respiratory irritation in individuals with sensitive airways. It was estimated in one major study that the excess risk of total mortality is 6.2% per each increase in 10pgPM2.s/m and 9.3% for cardiopulmonary mortality. ... 

---