Mediaction and Treatment for Copd

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Medication and Treatment for COPD
Inhaled Therapies
NICE COPD guidelines have made specific recommendations regarding the use of inhaled long-acting bronchodilators and inhaled steroids separately and in combination, but newer studies have assessed these drugs singly and in combination over longer periods of time. Bronchodilators (relievers)

Short-acting beta2 agonists (SABA)
Beta2 agonists act directly on bronchial smooth muscle to cause bronchodilation. They are the most widely used bronchodilators for COPD. Short-acting beta2 agonists are the most commonly used short-acting bronchodilators in COPD. EXAMPLES: Salbutamol or Bricanyal

Short-acting Anticholinergic (SAMA)
Cholinergic nerves are the main neural bronchoconstrictor pathway in the airways and the resting tone is increased in patients with COPD. Anticholinergic drugs cause bronchodilatation by blocking this bronchoconstrictor effect. Cholinergic effects on the airway are mediated by muscarinic receptors and these also mediate effects on mucus secretion. Anticholinergic drugs are also referred to as muscarinic antagonists (e.g. short-acting muscarinic antagonist (SAMA)). EXAMPLES: Atrovent (Ipratropium Bromide)

Short-acting bronchodilators, as necessary, should be the initial first-hand treatment for the relief of breathlessness and exercise limitation.

Long-acting beta2 agonists (LABA)
The bronchodilator effects of long-acting beta2 agonists are similar to the short-acting agents but their duration of action is around 12 hours. There are two long-acting beta2 agonists: salmeterol and formoterol. These drugs have quite different molecular structures and there are thought to be different mechanisms responsible for the longer duration of action of these two molecules.

Long-acting anticholinergic (long-acting muscarinic antagonists or LAMA) Tiotropium is currently the only long-acting anticholinergic bronchodilator available. Its duration of action is such that it can be given once daily.

Corticosteroids (Preventers)
There is little evidence that inhaled steroids have any effects on the inflammatory cells present in COPD: neutrophils, unlike eosinophils are relatively insensitive to the effects of steroids. Even high doses of inhaled steroids do not reduce the number of inflammatory cells or the levels of cytokines . Currently up to 70% of patients with COPD are prescribed an inhaled steroid and approximately 5% are prescribed oral steroids. The rationale for this is unclear and at least some of this prescribing may have been based on an extrapolation from the effects of these drugs in asthma and their effects at the time of an exacerbation. EXAMPLES: Fluticasone, Budesonide, Triamcinolone, Flunisolide, Beclomethasone.

Combination therapy
Since beta2-agonists, anticholinergic drugs and ICS affect airway calibre and lung function through different mechanisms combining drugs of these classes may potentially give clinical benefits to patients. An additional advantage of this approach is the ability to limit potential side effects of the drugs by avoiding having to use individual drugs near the top of their dose response curves. This involves Long-acting beta2 agonists (LABA) and inhaled corticosteroids (ICS). EXAMPLES: Seretide (Salmetrol/ Fluticasone) and Symbicort (Formoterol/Budesonide) Discontinued if not benefit after 4 weeks

Oral Therapies

Oral corticosteroids are more likely to cause side effects than inhaled corticosteroids because they are carried to all parts of the body. Inhaled corticosteroids only go to the lungs EXAMPLES: prednisone, prednisolone, dexamethasone and methylprednisolone

Also known as dimethyl xanthine, is a methyl xanthine drug used in therapy for respiratory diseases such as COPD and asthma under a variety of brand names. Because of its numerous side-effects, the drug is now rarely administered for clinical use. As a member of the xanthine family, it bears structural and...
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