Of COPD

Usually, it takes years of toxin exposure to cause the pathological alterations seen in COPD. In most cases, the disease is already well-progressed when COPD is diagnosed. Reversal of established chronic inflammatory disease is always extremely difficult to achieve and at present healing of COPD is impossible. Smoking cessation is the single most effective and cost-effective... 

The use of antibiotics is not recommended, except for the treatment of infectious exacerbations of COPD and other bacterial infections. Influenza vaccines decrease illness and death in COPD patients. Pneumococcal vaccination is also recommended. 

Up to 30% of COPD patients suffer from anxiety disorder or depression, and should be treated with conventional pharmacotherapy. 

Ms. Smith, age 68 years, returned to the clinic for a follow-up visit after receiving a diagnosis of COPD. She is taking theophylline daily and using a metered-dose inhaler 4 times a day. Determine what assessments would be most important for you to make at this time. 

O Inflammation plays a key role in the pathophysiology of COPD, but it differs from that seen in asthma therefore, the use of and response to anti-inflammatory medications are different. 

Inflammation is present in the lungs of all smokers. It is unclear why only 15% to 20% of smokers develop COPD, but susceptible individuals appear to have an exaggerated inflammatory response.5 O The inflammation of COPD differs from that seen in asthma, so the use of anti-inflammatory medications and the response to those medications are different. The inflammation of asthma is mainly mediated through eosinophils and mast cells. In COPD the primary inflammatory cells include neutrophils, macrophages, and CD8+ T lymphocytes. 

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

A suspected diagnosis of COPD should be based on the patient s symptoms and/or history of exposure to risk factors. Spirometry is required to confirm the diagnosis. The presence of a postbronchodilator FEV,/FVC ratio less than 70% [the ratio of FEV, to forced vital capacity (FVC)] confirms the presence of airflow limitation that is not fully reversible.1,2 Spirometry results can further be used to classify COPD severity (Table 12-1). Full pulmonary function tests (PFTs) with lung volumes and diffusion capacity and arterial blood gases are not necessary to establish the diagnosis or severity of COPD. 

Upon discontinuation of inhaled corticosteroids some patients may experience deterioration in lung function and an increase in dyspnea and mild exacerbations it is reasonable to reinstitute the medication in these patients.25 Completion of ongoing clinical trials assessing mortality should help to clarify the role of corticosteroid treatment of COPD. 

TABLE 12-5. Recommended Antibiotic Therapy in Acute Exacerbations of COPD... 

Family history of COPD or other chronic respiratory disease... 

The three-function model introduced in the preceding section has been established on an H-mordenite (HMOR) supported cobalt—palladium catalyst [12], For the sake of demonstration, model catalysts with a unique function, i.e. FI, F2 or F3, (Figure 5.1), were prepared to separately give evidence of the major role of each active site (Figure 5.1). Let us note that three functions does not necessarily mean three different active sites, but in the case of CoPd/HMOR material, three different sites were identified. 

Case of CoPd/HMOR (three-function catalyst Cat V) [12]... 

Initial symptoms of COPD include chronic cough and sputum production patients may have these symptoms for several years before dyspnea develops. The physical examination is normal in most patients who present in the milder stages of COPD. When airflow limitation becomes severe, patients may have cyanosis of mucosal membranes, development of a barrel chest due to hyperinflation of the lungs, an increased resting respiratory rate, shallow breathing, pursing of the lips during expiration, and use of accessory respiratory muscles. 

The diagnosis of COPD is based in part on the patient s symptoms and a history of exposure to risk factors such as tobacco smoke and occupational exposures. 

Assessment of airflow limitation through spirometry is the standard for diagnosing and monitoring COPD. The forced expiratory volume after 1 second (FEVj) is generally reduced except in very mild disease. The forced vital capacity (FVC) may also be decreased. The hallmark of COPD is a reduced FEVpFVC ratio to less than 70%. A postbronchodilator LEV, that is less than 80% of predicted confirms the presence of airflow limitation that is not fully reversible. 

Peak expiratory flow measurements are not adequate for diagnosis of COPD because of low specificity and a high degree of effort dependence. However, a low peak expiratory flow is consistent with COPD. 

Smoking cessation is the most effective strategy to reduce the risk of developing COPD and the only intervention proven to affect the longterm decline in FEVj and slow the progression of COPD. 

A combination product containing albuterol and ipratropium (Combi-vent) is available as an MDI for chronic maintenance therapy of COPD. Other similar combination products may become available in the future. 

The clinical benefits of systemic corticosteroid therapy in the chronic management of COPD are often not evident, and there is a high risk of toxicity. Consequently, chronic, systemic corticosteroids should be avoided if possible. 

The goals of therapy for patients experiencing exacerbations of COPD are prevention of hospitalization or reduction in length of hospital stay, prevention of acute respiratory failure and death, resolution of symptoms, and a return to baseline clinical status and quality of life. 

Although most exacerbations of COPD are thought to be caused by viral or bacterial infections, as many as 30% of exacerbations are caused by unknown factors. 

Selection of empiric antimicrobial therapy should be based on the most likely organisms. The most common organisms for acute exacerbation of COPD are Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae, and H. parainfluenzae. 

In acute exacerbations of COPD, white blood cell count, vital signs, chest x-ray, and changes in frequency of dyspnea, sputum volume, and sputum purulence should be assessed at the onset and throughout the exacerbation. In more severe exacerbations, arterial blood gases and oxygen saturation should also be monitored. 

At Paco2 of 5 kPa The line should demonstrate that, under normal conditions, the minute volume (MV) remains relatively constant around 6 l.min 1 until the Pao2 falls below 8 kPa. Show that the rise in MV following this is extremely steep. This illustrates the hypoxic drive, which is so often talked about in the setting of COPD. 

COPD is a progressive obstruction of the airways as a consequence of small airway disease and emphysema.It is the fourth leading cause of death in developed countries. Chronic inflammation and regulated air supply in the airway are amplified in case of COPD. Decreased activity of histone deacetylase is observed in chronic obstructive pulmonary disease. ... 

Normally corticosteroids are used for COPD treatment. The corticosteroids bind to glucocorticoid receptors and enter the nucleus of the cells, where it recruits HDAC-2. HDAC-2 deacetylates the chromatin and represses gene expression of inflammatory genes. Thus, low levels of HDAC-2 is detrimental to the treatment of COPD. Antioxidants (for removal of superoxides) or iNOS inhibitor or theophylline/curcumin for PI3K inhibition are some of the options to restore the required HDAC-2 level. 

Hansel TT, Barnes PJ, Tiotropium bromide A novel once-daily anticholinergic bronchodilator for the treatment of COPD, Drugs Today (Bare) 38 585-600, 2002. 

Maintenance treatment of COPD - The usual dosage is the inhalation of the contents of one 12 meg formoterol capsule every 12 hours using the Aerolizer Inhaler. 

Chronic obstructive pulmonary disease (COPD) associated with chronic bronchitis For the twice-daily maintenance treatment of airflow obstruction in patients with COPD associated with chronic bronchitis. Fluticasone propionate/salmeterol 250 meg per 50 meg twice daily is the only approved dosage for the treatment of COPD associated with chronic bronchitis. Fligher doses, including fluticasone propionate/salmeterol 500 meg per 50 meg, are not recommended. 

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