VIFEX SYRUP

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

• Chronic bronchitis
• Asthma
• Chronic obstructive pulmonary disease (COPD)
• Respiratory tract infections with thick mucus

Dosage

Children: Refer to BNF for Children for specific dosing guidelines based on age and weight.

Adults: The usual oral dosage is 8 to 16 mg three times daily. The dosage may be adjusted according to the severity of the condition and patient response.

Mechanism of action

Bromohexine acts by increasing the production of surfactant in the alveoli and enhancing the secretion of mucus in the respiratory tract. It promotes the hydrolysis of mucopolysaccharides and stimulates the ciliary activity of the respiratory epithelium, leading to increased mucus clearance. This action is facilitated through its effect on serous glands in the bronchial mucosa, thereby reducing mucus viscosity and enhancing expectoration.

Pharmacodynamics

Bromohexine exhibits mucolytic and expectorant properties. It alters the viscosity of mucus, making it less thick and easier to clear from the airways. Its action on the respiratory tract aids in improving airflow and alleviating symptoms associated with respiratory disorders such as chronic bronchitis and asthma. The onset of action typically occurs within a few hours of administration, with a duration of effect that can last several hours.

Pharmacokinetics

Bromohexine is well absorbed after oral administration, with peak plasma concentrations occurring within 1 to 2 hours. It is metabolized in the liver to form active metabolites. The elimination half-life is approximately 8 to 12 hours, and it is primarily excreted in the urine as metabolites and unchanged drug. The drug's bioavailability can be affected by food, with higher absorption rates observed when taken on an empty stomach.

Adverse effects

• Gastrointestinal disturbances
• Allergic reactions including rash and pruritus
• Headache
• Dizziness

Precautions

• Caution in patients with peptic ulcer disease
• Use with caution in patients with asthma or other respiratory conditions

Pregnancy

There is limited data on the safety of bromohexine in pregnancy. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Bromohexine is excreted in breast milk. Caution should be exercised when administering to nursing mothers.

Storage

Store in a cool, dry place, away from direct sunlight.

Formulations

• Oral solution
• Tablets
• Syrup

Indications

• Chest congestion
• Productive cough
• Respiratory infections
• Common cold
• Allergic rhinitis

Dosage

Children: Refer to the BNF for Children for specific dosing information.

Adults: Refer to the BNF for specific dosing information.

Mechanism of action

Guaifenesin acts as an expectorant by increasing the volume and reducing the viscosity of secretions in the respiratory tract. This promotes mucociliary clearance, facilitating the expulsion of mucus and reducing productive cough.

Pharmacodynamics

Guaifenesin enhances the output of respiratory tract fluid, which helps to clear mucus and phlegm. This action can lead to increased hydration of the respiratory mucosa, improving ciliary function and promoting the clearance of mucus from the airways.

Pharmacokinetics

Guaifenesin is rapidly absorbed from the gastrointestinal tract. It is metabolized in the liver and primarily excreted in the urine as inactive metabolites. The half-life of guaifenesin is approximately one hour.

Adverse effects

• Nausea
• Vomiting
• Dizziness
• Headache
• Rash
• Diarrhea

Precautions

• Caution in patients with respiratory conditions
• Ensure adequate hydration during use

Pregnancy

Guaifenesin is categorized as pregnancy category C. Use during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Guaifenesin is excreted in breast milk. Caution is advised when administered to nursing mothers.

Storage

Store at room temperature, away from moisture and heat. Keep out of reach of children.

Formulations

• Oral tablets
• Oral syrup
• Extended-release formulations

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.