preview

Q & A Case Study On Salbutamol

Good Essays
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 • Largely superseded in chronic prophylactic therapy of ‘allergic asthma’ by…show more content…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
Get Access