SALBUCORT

Indications

• Asthma
• Chronic obstructive pulmonary disease (COPD)
• Exercise-induced bronchospasm
• Other conditions associated with reversible airways obstruction

Dosage

Children: Child 5–11 years: 2.5 mg via nebulisation or 50 micrograms by inhalation; Child 12–17 years: 5 mg via nebulisation or

Adults: 500 micrograms every 4 hours if required, or 50 micrograms by inhalation twice daily, with possible increase to 100 micrograms twice daily in more severe cases.

Mechanism of action

Salbutamol preferentially binds to beta-2 adrenergic receptors, stimulating adenyl cyclase and increasing intracellular cyclic AMP. This results in protein kinase A activation, which inhibits myosin phosphorylation and reduces intracellular calcium concentrations, leading to smooth muscle relaxation in the airways. Additionally, increased cyclic AMP inhibits the release of inflammatory mediators from mast cells.

Pharmacodynamics

Salbutamol is known for its bronchodilatory effects, particularly in asthma and chronic obstructive pulmonary disease (COPD). It selectively stimulates beta-2 receptors, which are predominantly located in bronchial smooth muscle. The drug is effective in providing rapid relief from bronchospasm and has been shown to prevent exercise-induced bronchospasm. The R-isomer of salbutamol is primarily responsible for its therapeutic effects, while the S-isomer may contribute to side effects. Salbutamol may also induce metabolic effects, such as hyperglycemia.

Pharmacokinetics

Salbutamol is administered via inhalation, with onset of action typically occurring within minutes. Its duration of action is around 4 to 6 hours for the immediate-release formulation. The drug undergoes hepatic metabolism and is excreted primarily in urine. Its pharmacokinetic profile can vary based on the route of administration, with inhalation providing faster and more localized effects compared to oral or parenteral routes.

Adverse effects

• Tremors
• Nervousness
• Palpitations
• Tachycardia
• Headache
• Dizziness
• Nausea
• Hypokalemia
• Increased blood glucose levels

Interactions

• Other beta-agonists
• Beta-blockers
• Diuretics
• Monoamine oxidase inhibitors (MAOIs)
• Thyroid hormones
• Caffeine

Precautions

• Use with caution in patients with cardiovascular disorders
• Hypertension
• Hyperthyroidism
• Diabetes mellitus
• Seizure disorders
• Pregnancy and breastfeeding

Pregnancy

Inhaled drugs for asthma can be taken as normal during pregnancy.

Breast-feeding

Inhaled drugs for asthma can be taken as normal during breastfeeding.

Storage

Store below 25 degrees Celsius. Protect from light and moisture.

Formulations

• Inhalation aerosol
• Inhalation solution
• Inhalation powder

Indications

• Asthma
• Chronic Obstructive Pulmonary Disease (COPD)
• Allergic Rhinitis
• Cystic Fibrosis
• Pulmonary Hypertension

Dosage

Children: Refer to specific inhaled medication guidelines for paediatric dosing.

Adults: Refer to specific inhaled medication guidelines for adult dosing.

Mechanism of action

Inhaled medications can have various mechanisms of action depending on the specific drug. For example, beta-2 adrenergic agonists stimulate beta-2 receptors on bronchial smooth muscle, leading to bronchodilation. Corticosteroids inhibit the expression of inflammatory mediators and reduce airway inflammation, while anticholinergics block acetylcholine from binding to its receptors, resulting in decreased bronchoconstriction.

Pharmacodynamics

The pharmacodynamics of inhaled medications involve their interaction with specific receptors or pathways in the lungs. Bronchodilators cause relaxation of the bronchial smooth muscle, leading to increased airflow. Corticosteroids effectively reduce inflammation and mucus production in the airways, thereby improving respiratory function and reducing exacerbations of asthma and COPD. The rapid delivery of these drugs to the site of action enhances their efficacy.

Pharmacokinetics

Inhaled medications have distinct pharmacokinetic properties. The onset of action can be very rapid, often within minutes, due to direct delivery to the lungs. The bioavailability depends on factors such as particle size, inhalation technique, and the type of inhaler used. Systemic absorption is generally lower than with oral medications, which minimizes systemic side effects. The duration of action varies based on the specific drug class; for example, short-acting beta agonists provide quick relief, while long-acting agents offer prolonged effects.

Pregnancy

Consult healthcare provider for risk assessment and guidance, as safety data may vary depending on the specific inhalation formulation.

Breast-feeding

Consult healthcare provider, as some inhalation medications may be excreted in breast milk and could affect the infant.

Storage

Store in a cool, dry place away from direct sunlight. Check specific product guidelines for temperature and humidity requirements.

Indications

• Asthma
• Chronic Obstructive Pulmonary Disease (COPD)
• Allergic Rhinitis
• Acute Bronchospasm
• Exercise-Induced Bronchospasm

Dosage

Children: Refer to the BNF for Children for specific paediatric dosing information, as it varies by medication and condition.

Adults: Refer to the specific product information for adult dosing, as it varies by medication and condition.

Mechanism of action

Pressurized drug delivery systems, such as metered-dose inhalers (MDIs), utilize propellants to create an aerosolized mist of medication. The active pharmaceutical ingredient is usually a bronchodilator, corticosteroid, or a combination, which works by relaxing bronchial smooth muscles, reducing inflammation, and improving airflow in the lungs.

Pharmacodynamics

The pharmacodynamics of pressurized inhalation therapies depend on the specific drug used. For instance, beta-2 adrenergic agonists lead to bronchodilation by stimulating beta-2 receptors in the bronchial smooth muscle, while corticosteroids reduce inflammation by inhibiting various inflammatory processes and immune responses in the airways.

Pharmacokinetics

The pharmacokinetics of drugs delivered via pressurized systems varies widely depending on the active ingredient. Generally, the onset of action is rapid due to direct delivery to the lungs, with peak effects occurring within minutes to hours. Systemic absorption may occur, though this is often limited compared to oral or intravenous routes. The half-life, metabolism, and excretion depend on the specific drug component.

Pregnancy

Use during pregnancy only if clearly needed. Assess the risks and benefits with a healthcare provider.

Breast-feeding

Use with caution. Monitor the infant for potential side effects.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Mechanism of action

In vitro studies and in vivo pharmacologic studies have shown that salbutamol has a preferential effect on beta2-adrenergic receptors compared with isoproterenol. Although beta2­ adrenoceptors are the predominant adrenergic receptors in bronchial smooth muscle and beta1 adrenoceptors are the predominant receptors in the heart, there are also beta2-adrenoceptors in the human heart comprising 10% to 50% of the total beta-adrenoceptors. The precise function of these receptors has not been established, but their presence raises the possibility that even selective beta2-agonists may have cardiac effects. Activation of beta2-adrenergic receptors on airway smooth muscle leads to the activation of adenyl cyclase and to an increase in the intracellular concentration of cyclic-3′,5′-adenosine monophosphate (cyclic AMP). This increase of cyclic AMP leads to the activation of protein kinase A, which inhibits the phosphorylation of myosin and lowers intracellular ionic calcium concentrations, resulting in relaxation. Salbutamol relaxes the smooth muscles of all airways, from the trachea to the terminal bronchioles. Salbutamol acts as a functional antagonist to relax the airway irrespective of the spasmogen involved, thus protecting against all bronchoconstrictor challenges. Increased cyclic AMP concentrations are also associated with the inhibition of release of mediators from mast cells in the airway. Salbutamol has been shown in most controlled clinical trials to have more effect on the respiratory tract, in the form of bronchial smooth muscle relaxation, than isoproterenol at comparable doses while producing fewer cardiovascular effects. Controlled clinical studies and other clinical experience have shown that inhaled albuterol, like other beta-adrenergic agonist drugs, can produce a significant cardiovascular effect in some patients, as measured by pulse rate, blood pressure, symptoms, and/or electrocardiographic changes. A measurable decrease in airway resistance is typically observed within 5 to 15 minutes after inhalation of salbutamol. The maximum improvement in pulmonary function usually occurs 60 to 90 minutes after salbutamol treatment, and significant bronchodilator activity has been observed to persist for 3 to 6 hours. Adrenergic bronchodilators act by stimulating beta2-adrenergic receptors in the lungs to relax bronchial smooth muscle, thereby relieving bronchospasm. /Adrenergic bronchodilators/ Primarily stimulates beta2-adrenergic receptors, with some minor beta1-adrenergic activity. In vitro studies and in vivo pharmacologic studies have demonstrated that albuterol has a preferential effect on beta2-adrenergic receptors compared with isoproterenol. While it is recognized that beta2-adrenergic receptors are the predominant receptors in bronchial smooth muscle, date indicate that there is a population of beta2-receptors in the human heart existing in a concentration between 10% and 50% of cardiac beta-adrenergic receptors. The precise function of these receptors has not been established. Activation of beta2-adrenergic receptors on airway smooth muscle leads to the activation of adenylcyclase and to an increase in the intracellular concentration of cyclic-3',5'-adenosine monophosphate (cyclic AMP). This increase of cyclic AMP leads to the activation of protein kinase A, which inhibits the phosphorylation of myosin and lowers intracellular ionic calcium concentrations, resulting in relaxation. Albuterol relaxes the smooth muscles of all airways, from the trachea to the terminal bronchioles. Albuterol acts as a functional antagonist to relax the airway irrespective of the spasmogen involved, this protecting against all bronchoconstrictor challenges. Increased cyclic AMP concentrations are also associated with the inhibition of release of mediators from most cells in the airway.

Pharmacodynamics

Salbutamol (INN) or albuterol (USAN), a moderately selective beta(2)-receptor agonist similar in structure to terbutaline, is widely used as a bronchodilator to manage asthma and other chronic obstructive airway diseases. The R-isomer, levalbuterol, is responsible for bronchodilation while the S-isomer increases bronchial reactivity. The R-enantiomer is available and sold in its pure form as levalbuterol and subsequently may produce fewer side-effects with only the R-enantiomer present - although this has not been formally demonstrated. After oral and parenteral administration, stimulation of the beta receptors in the body, both beta-1 and beta-2, occurs because (a) beta-2 selectivity is not absolute, and (b) higher concentrations of salbutamol occur in the regions of these receptors with these modes of administration. This results in the beta-1 effect of cardiac stimulation, though not so much as with isoprenaline, and beta-2 effects of peripheral vasodilatation and hypotension, skeletal muscle tremor, and uterine muscle relaxation. Metabolic effects such as hyperinsulinemia and hyperglycemia also may occur, although it is not known whether these effects are mediated by beta-1 or beta-2 receptors. The serum potassium levels have a tendency to fall.