sustainable use of drugs in bronchoobstructive sindrome

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slide 1 sustainable use of drugs in bronchoobstructive sindrome bronchial asthma the term asthma is derived from the greek word meaning difficulty in breathing. asthma is a chronic inflammatory allergic disease: the patients suffer with reversible episodes of airways obstruction due to bronchial hyper-responsiveness. in the early (acute) phase there are smooth muscle spasm and excessive bronchial secretion of mucus. in the late (chronic or delayed) phase, inflammation continues, accompanied by fibrosis, oedema and necrosis of bronchial epithelial cells. factors that exacerbate asthma the cardinal symptoms of asthma are breathlessness wheezing, cough and chest tightness with worsening of these symptoms at night. in the acute attack there are ra- pid respiratory rate and tachycardia. the majority of patients suffer with atopic extrinsic asthma, which is associated with exposure to specific allergen (pollen or house-dust mite) . in non-atopic extrinsic asthma the attack may be stimulated with some non-specific stimulus, e.g. …

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ronchospasm precipitated by uncompensated congestive heart failure. pathophysiology of asthma antigens (pollen and house-dust mites) sensitize patients by eliciting the production of ige type of antibodies, which remain either circulating in the blood or become attached to the mast cells of nasal or bronchial tissues and basophils. on re-exposure the same antigen, the resulting antigen- antibody reaction in the early phase causes degranulation of the lung mast cells and releasing of the powerful bronchoconstrictors: histamine, 5-ht, pgd2 and cysteinyl leucotriens (ltb4, ltc4 and ltd4). lung mast cells also release ils (il-4, il-5 and il-13). in the late (delayed) phase of asthma, these mediators activate additional inflammatory cells (eosinophils, basophils, and alveolar macrophages) which also release lts and ils. other mediators of inflammation, in delayed phase, are: adenosine (causing bronchconstriction), neuropeptides (sp, causing mucus secretion and increase in vascular permeability; neurokinin a, causing bronchoconstriction), paf etc. the normal tone of bronchial …

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m, tiotropium, oxitropium methyl xanthines: theophylline, aminophylline, theotard 2. mast cell stabilizers: sodium cromoglycate, ketotifen, nedocromil 3. glucocorticosteroids (gcs) oral: prednisone, methylprednisolone parenteral: methylprednisolone, betamethasone inhalational: beclomethasone, budenoside, fluticasone, triamcinolone 4. inhalational β2-agonists/glucocorticosteroids seretide® (fluticasone/salmeterol) symbicort® (budenoside/formoterol) 5. leukotriene modulators 5-lipoxygenase inhibitor: zileuton ltd4-antgonists: zafirlukast, montelukast 6. monoclonal anti-ige antibody: omalizumab 7. miscellaneous: no-donors, calcium antagonists the common combination of chronic bronchitis and emphysema has also been termed chronic obstructive airways disease (coad) or chronic obstructive pulmonary disease (copd). this is a morbid condition characterized by non-reverseble bronchial obstruction caused by deformation and sclerosis of bronchial tree due to persistent inflammation. up to 20% of adults worldwide have the disease, and this proportion is higher in heavily industrialized countries. chronic bronchitis occurs in the majority of heavy smokers, but significant airway obstruction or emphysema, or both occurs in only a minority. it is the third most common cause of death …

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given via nasal cannulae. occasionally transtracheal oxygen therapy (ttot) via a small polyethylene catheter introduced directly into the trachea. long-term oxygen therapy from cylinders or an oxygen concentrator may be of value in patients with chronic stable respiratory failure. the flow rate and concentration are adjusted to relieve arterial hypoxaemia while avoiding carbon dioxide narcosis. infections are frequent, and it is important to educate patients in the early recognition of symptoms and signs, for example change of sputum colour and quality, fever or increasing wheeze. many patients should be given a supply of antibiotics to keep at home for self-medication. bronchodilators – relievers (β-agonists, m-cholinolytics, methyl xanthins) provide a rapid sympto- matic relief but they do not control the disease process. selective β2-agonists activate β2-receptors present on airway smooth muscle and mast cells too. these agents relax airway smooth muscle, inhibit the release of bronchoconstricting mediators from the adipocytes and …

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anthines (theophylline, aminophylline, theotard): a) inhibit phosphodiesterase iii (present in airway muscle) and iv (present in eosinophil and mast cells), the two specific isoenzymes responsible for the degradation of camp; b) block the adenosine-1-receptors on airway muscle and adenosine-3-receptors, present on mast cells. the main use of methyl xanthins is in the management of asthma and copd (chronic obstructive pulmonary disease), usually as combination therapy with beta-2-agonists. glucocorticosteroids provide long-term stabilization of the symptoms due to their anti-inflammatory effects. inhaled gcs, along with beta-2-agonists are the first choice drugs for chronic asthma. gcs inhibit the release of pgs and lts and thus prevent smooth muscle contraction, vascular permeability and airway mucus secretion. gcs produce eosinopenia which prevents cytotoxic effects of the mediators released from eosinophils. gcs enhance beta-2-adrenergic response by up-regulating the beta-2-receptors in lung cells and leuckocytes. several hours are required for dna transcription and rna translation to occur …

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slide 1 sustainable use of drugs in bronchoobstructive sindrome bronchial asthma the term asthma is derived from the greek word meaning difficulty in breathing. asthma is a chronic inflammatory allergic disease: the patients suffer with reversible episodes of airways obstruction due to bronchial hyper-responsiveness. in the early (acute) phase there are smooth muscle spasm and excessive bronchial secretion of mucus. in the late (chronic or delayed) phase, inflammation continues, accompanied by fibrosis, oedema and necrosis of bronchial epithelial cells. factors that exacerbate asthma the cardinal symptoms of asthma are breathlessness wheezing, cough and chest tightness with worsening of these symptoms at night. in the acute attack there are ra- pid respiratory rate and tachycardia. the maj...

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