Q & A Case Study On Salbutamol

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Salbutamol undergoes considerable presystemic metabolism in the intestinal mucosa (sulphation) and hepatic conjugation to form an inactive metabolite that is excreted in the urine. Most (approximately 90%) of the dose administered by aerosol is swallowed, but the 10–15% which is inhaled largely remains as free drug in the airways. The plasma elimination half-life (t1/2) is two to four hours. Salmeterol is long acting, with a duration of action of at least 12 hours, allowing twice daily administration. The lipophilic side-chain of salmeterol binds firmly to an exo-site that is adjacent to, but distinct from, the β2-agonist binding site. Consequently, salmeterol functions as an almost irreversible agonist. The onset of bronchodilatation is slow…show more content…
May be used in children to avoid systemic steroids 3 Fluticasone 18 1200 May cause fewer systemic side effects than others  Adverse effects of inhaled steroids • At the lowest recommended daily dose for adults, there is no prolonged suppression of the hypothalamic–pituitary– adrenal (HPA) axis. Higher doses can produce clinically important depression of adrenal function. • Candidiasis of the pharynx or larynx occurs in 10–15% of patients. Using the minimum effective dose, or a ‘spacer device’, or gargling/using mouthwashes after dosing, minimizes this problem. • A hoarse voice may develop due to a laryngeal myopathy at high doses. This is reversible and its occurrence is minimized by the use of a ‘spacer’. • Bruising and skin atrophy occur at high doses. • Inhibition of long bone growth during prolonged high dose treatment in children. • Posterior subcapsular cataracts may develop following prolonged use. 5.2.2 Mast Cell Stabilizers: e.g. Sodium cromoglicate, Nedocromil sodium. • Its mechanism of action is unclear. It has an anti-inflammatory effect. • Largely superseded in chronic prophylactic therapy of ‘allergic asthma’ by…show more content…
Leukotrienes (LT) are fatty acid-derived mediators containing a conjugated triene structure. They are formed when arachidonic acid (Chapter 26) is liberated from the cell membrane of cells, as a result of cell activation by allergic or other noxious stimuli. 5-Lipoxygenase is the enzyme required for the synthesis of LTA4, which is an unstable epoxide precursor of the two subgroups of biologically important leukotrienes. LTB4 is a dihydroxy 20-carbon-atom fatty acid which is a potent pro-inflammatory chemo-attractant. The other group is the cysteinyl leukotrienes (LTC4, LTD4 and LTE4). LTC4 is a conjugate of LTA4 plus glutathione, a tripeptide which combines with LTA4 via its cysteine residue. LTC4 is converted to an active metabolite (LTD4) by the removal of the terminal amino acid in the peptide side-chain. Removal of a second amino acid results in a less active metabolite (LTE4). LTC4, LTD4 and LTE4, the ‘sulphidopeptide leukotrienes’ or ‘cysteinyl leukotrienes’, collectively account for the activity that used to be referred to as ‘slow-reacting substance of anaphylaxis’ (SRS-A). They all (but especially LTD4) bind to the Cys-LT1 receptor to cause bronchoconstriction, attraction of eosinophils and production of

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