BRONCHOPED

Indications

• Asthma
• Chronic Obstructive Pulmonary Disease (COPD)
• Exacerbation of reversible airways obstruction
• Prevention of exercise-induced bronchospasm
• Uncomplicated premature labor (under specialist supervision)

Dosage

Adults: Initially 2.5 mg 3 times a day for 1–2 weeks, then increased to

Mechanism of action

Terbutaline exerts its effects by selectively stimulating beta-2 adrenergic receptors located in the smooth muscle of the airways. This activation leads to the activation of adenylate cyclase, resulting in increased levels of cyclic AMP (cAMP). Elevated cAMP levels promote relaxation of the bronchial smooth muscle, leading to bronchodilation. Additionally, terbutaline may inhibit the release of mediators from mast cells, reducing bronchoconstriction and inflammation.

Pharmacodynamics

The pharmacodynamic profile of terbutaline includes rapid onset of action, typically within 5 to 15 minutes when inhaled, and a duration of action of approximately 3 to 6 hours. It provides symptomatic relief from bronchospasm associated with asthma and chronic obstructive pulmonary disease (COPD). The drug is also noted for its tocolytic effects, as it can inhibit uterine contractions, making it useful in managing premature labor.

Pharmacokinetics

Terbutaline is well absorbed following inhalation and oral administration, with peak plasma concentrations occurring within 1 to 3 hours. It exhibits a volume of distribution of approximately 3 L/kg, indicating extensive tissue distribution. The drug is metabolized primarily in the liver and has a half-life of about 3 to 5 hours. Terbutaline is excreted mainly in urine, both as unchanged drug and metabolites. Its pharmacokinetic profile may be affected by factors such as age, liver function, and concomitant medications.

Adverse effects

• Tachycardia
• Palpitations
• Tremors
• Headache
• Nausea
• Dizziness
• Hypokalemia
• Hyperglycemia

Interactions

• Beta-blockers may reduce the effectiveness of terbutaline
• Corticosteroids may enhance the effect of terbutaline
• Concomitant use with other sympathomimetics may increase cardiovascular side effects

Precautions

• Use with caution in patients with cardiovascular disorders
• Caution in patients with diabetes due to potential hyperglycemia
• Monitor potassium levels in patients at risk of hypokalemia
• Monitor for paradoxical bronchospasm

Pregnancy

Terbutaline should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Terbutaline 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. Keep out of reach of children.

Formulations

• Tablets: 2.5 mg and 5 mg
• Nebuliser solution: 0.5 mg/ml
• Injection: 0.5 mg/1 ml

Indications

• Nitrogen supplementation in clinical nutrition
• Management of metabolic alkalosis
• Treatment of certain types of kidney disorders

Dosage

Children: Specific pediatric dosing information is not detailed in the BNF. Refer to the BNF for Children for appropriate dosing based on age and condition.

Adults: Dosage varies based on clinical indication and should be guided by specific treatment protocols. Refer to clinical guidelines for detailed dosing information.

Mechanism of action

Ammonium ions participate in various metabolic pathways, including the biosynthesis of amino acids and nucleotides. It serves as a nitrogen source for organisms, facilitating the synthesis of essential biomolecules. The presence of ammonium can influence pH levels and osmotic balance within cells, thereby affecting cellular functions and enzyme activities.

Pharmacodynamics

Ammonium affects cellular metabolism by acting as a nitrogen donor in the synthesis of organic compounds. Its role in the nitrogen cycle and as a substrate in biochemical pathways allows for the maintenance of cellular functions, including energy production and cellular growth. Alterations in ammonium levels can influence various physiological processes, including neurotransmitter synthesis and energy metabolism.

Pharmacokinetics

Ammonium is readily absorbed and distributed in biological systems. It can be produced endogenously through amino acid metabolism or obtained from dietary sources. The excretion of ammonium primarily occurs through the kidneys, where it is converted to urea for elimination. Ammonium levels are regulated by various mechanisms, including the action of renal tubular cells that either secrete or reabsorb ammonium based on the body's needs.

Indications

• Cough associated with respiratory tract infections
• Acid-base disorders
• Edema management

Dosage

Children: Refer to the BNF for Children for appropriate paediatric dosing guidelines based on age and condition.

Adults: Refer to the BNF for specific adult dosing guidelines as they depend on the indication and clinical context.

Mechanism of action

Ammonium chloride increases acidity by raising hydrogen ion concentrations. It dissociates into ammonium and chloride ions; the ammonium is converted to urea in the liver, releasing hydrogen ions that lower pH. The chloride ions displace bicarbonate in extracellular fluid, leading to acidosis and increased renal excretion of electrolytes and water, resulting in fluid mobilization.

Pharmacodynamics

Ammonium chloride acts as a systemic acidifier, facilitating the excretion of chloride and sodium, while also increasing the acidity of body fluids. The conversion of ammonium to urea in the liver with the release of hydrogen ions contributes to a decrease in blood pH, affecting acid-base balance in the body.

Pharmacokinetics

Ammonium chloride is absorbed from the gastrointestinal tract and metabolized in the liver, where it is converted to urea. The dissociated ions impact renal function, leading to increased excretion of sodium, potassium, and water. The elimination half-life and specific metabolism details are not explicitly defined.

Adverse effects

• Nausea
• Vomiting
• Abdominal pain
• Diarrhea
• Dizziness
• Headache

Interactions

• Antacids may reduce the effectiveness of ammonium chloride
• Potassium-sparing diuretics may increase the risk of hyperkalemia

Precautions

• Use with caution in patients with renal impairment
• Monitor electrolyte levels during prolonged therapy
• Consider potential for acidosis in patients with liver disease

Pregnancy

Ammonium chloride should only be used during pregnancy if the potential benefit justifies the potential risk to the fetus. Consult a healthcare provider for individualized advice.

Breast-feeding

Ammonium chloride is excreted in breast milk. Use caution and consult a healthcare provider if breastfeeding.

Storage

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

Formulations

• Oral solution
• Powder for oral solution

Indications

• Bronchospasm
• Asthma
• Chronic bronchitis
• Emphysema

Dosage

Children: Refer to the BNF for Children for specific paediatric dosing recommendations.

Adults: Refer to the BNF for specific dosing guidelines.

Mechanism of action

Terbutaline exerts its effects through selective agonism of beta-2 adrenergic receptors located in the bronchioles. This activation leads to the stimulation of adenylyl cyclase, which increases the levels of intracellular cyclic adenosine monophosphate (cAMP). The rise in cAMP reduces intracellular calcium concentrations, leading to the activation of protein kinase A. This enzyme inactivates myosin light-chain kinase and activates myosin light-chain phosphatase, ultimately resulting in the relaxation of smooth muscle within the bronchioles.

Pharmacodynamics

As a beta-2 adrenergic receptor agonist, terbutaline is indicated for the relief of bronchospasm in conditions such as asthma, chronic bronchitis, and emphysema. It has a rapid onset of action and a relatively short duration of effect, typically requiring administration up to three times daily in its inhaled form. The therapeutic window for terbutaline is wide, making it generally safe within prescribed doses.

Pharmacokinetics

Terbutaline is rapidly absorbed when administered via inhalation, allowing for quick therapeutic action. The drug undergoes extensive first-pass metabolism when taken orally, which may affect its bioavailability. It is primarily metabolized in the liver and has a half-life that supports frequent dosing. Excretion occurs mainly via the kidneys, with metabolites detectable in urine.

Contra-indications

• Hypersensitivity to terbutaline or any of its components
• Severe hypersensitivity to sympathomimetic amines
• Tachyarrhythmias
• Cardiac arrhythmias

Adverse effects

• Tremor
• Tachycardia
• Palpitations
• Headache
• Nausea
• Dizziness
• Muscle cramps
• Hypokalemia

Interactions

• Beta-blockers may reduce the effectiveness of terbutaline
• Concomitant use with other sympathomimetics may increase the risk of cardiovascular side effects
• Monoamine oxidase inhibitors (MAOIs) can potentiate the effects of terbutaline

Precautions

• Use with caution in patients with cardiovascular disorders
• Monitor potassium levels in patients with significant hypokalemia
• Caution in patients with diabetes mellitus as beta agonists may induce hyperglycemia

Pregnancy

Use during pregnancy only if the potential benefit justifies the potential risk to the fetus. Category C.

Breast-feeding

Terbutaline is excreted in human milk, and caution should be exercised when administered to a nursing woman.

Storage

Store below 25 degrees Celsius. Protect from light and moisture. Keep out of reach of children.

Formulations

• Inhalation aerosol
• Oral tablets
• Injection

Mechanism of action

Ammonium chloride increases acidity by increasing the amount of hydrogen ion concentrations. Ammonium chloride can be used as an expectorant due to its irritative action on the bronchial mucosa. This effect causes the production of respiratory tract fluid which in order facilitates the effective cough. The acid-forming properties of ammonium chloride result from dissociation of the salt to an ammonium cation and a chloride anion. In patients with normal hepatic function, the ammonium cation is converted to urea by the liver and a hydrogen cation is released which reacts with a bicarbonate ion to form water and carbon dioxide. The chloride anion combines with fixed bases in the extracellular fluid, thereby reducing the alkaline reserve of the body. The net result is the displacement of bicarbonate ions by chloride anions. The displacement of bicarbonate by chloride alters the bicarbonate:carbonic acid ratio if the body and acidosis results. The increased chloride concentration in the extracellular fluid produces an increased load to the renal tubules and appreciable amounts of chloride anions escape reabsorption. These anions are excreted along with cations and water. Sodium is the principal cation excreted; however, potassium excretion may also be increased to some degree. By increasing the excretion of both extracellular electrolytes and water, ammonium chloride causes a net loss of extracellular fluid and promotes the mobilization of edema fluid.

Pharmacodynamics

Systemic acidifier. In liver ammonium chloride is converted into urea with the liberation of hydrogen ions ( which lowers the pH) and chloride.

Mechanism of action

Terbutaline is a selective beta-2 adrenergic receptor agonist. Agonism of these receptors in bronchioles activates adenylyl cyclase, increasing intracellular cyclic adenosine monophosphate (cAMP). Increased cAMP decreases intracellular calcium, activating protein kinase A, inactivating myosin light-chain kinase, activating myosin light-chain phosphatase, and finally relaxing smooth muscle in the bronchiole.

Pharmacodynamics

Terbutaline is a beta-2 adrenergic receptor agonist indicated to treat reversibly bronchospasm in asthmatic patients with bronchitis and emphysema. It has a short duration as the inhaled form is taken up to three times daily, and the therapeutic window is wide.