COSCOPIN* PAEDIATRIC COMBINATION PRODUCT SYRUP

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

• Acidulant in food and beverages
• Preservative in pharmaceutical formulations
• pH adjuster in various chemical preparations

Dosage

Children: Refer to product-specific guidelines for appropriate dosing based on formulation and indication.

Adults: Refer to product-specific guidelines for appropriate dosing based on formulation and indication.

Mechanism of action

Citric acid acts by chelating metal ions, which can enhance the solubility of certain compounds and improve their bioavailability. It also contributes to the acidity of the environment, which can influence enzymatic activity and metabolic pathways, particularly in the degradation of citronellol.

Pharmacodynamics

Citric acid exhibits mild pharmacological effects primarily attributed to its role in metabolic processes. It aids in the regulation of pH levels, which can impact enzymatic reactions and biochemical pathways. The acid's chelating properties may help to reduce the toxicity of certain metal ions in biological systems.

Pharmacokinetics

Citric acid is rapidly absorbed after oral administration and is metabolized in the liver. It undergoes conversion to various metabolites in the citric acid cycle, contributing to energy production. The elimination primarily occurs through urine, with minimal accumulation in the body.

Pregnancy

Citric acid is generally regarded as safe during pregnancy when used in food amounts. However, consult a healthcare provider for advice on medicinal use.

Breast-feeding

Citric acid is considered safe during breastfeeding when consumed in food amounts. For medicinal use, consult a healthcare provider.

Storage

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

Indications

• Cough suppression
• Chronic cough
• Cough due to respiratory tract infections

Dosage

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

Adults: Refer to the BNF for specific adult dosing guidelines.

Mechanism of action

Noscapine exerts its antitussive effects primarily through its activity as a sigma receptor agonist. Experimental studies suggest that when sigma-specific antagonists, such as rimcazole, are administered prior to noscapine, there is a dose-dependent decrease in its antitussive efficacy, indicating that sigma receptor interaction is crucial for its cough-suppressing action.

Pharmacodynamics

Noscapine's pharmacodynamic profile is characterized by its ability to suppress the cough reflex without the sedative or addictive properties commonly associated with opioids. Its selective engagement with sigma receptors allows it to achieve its therapeutic effect while minimizing side effects on the central nervous system.

Pharmacokinetics

Noscapine is absorbed following oral administration, with peak plasma concentrations typically occurring within a few hours. It undergoes hepatic metabolism, which may affect its bioavailability and efficacy. The elimination half-life of noscapine is variable, but it is generally considered to have a moderate duration of action, necessitating multiple doses for sustained antitussive effect.

Adverse effects

• Nausea
• Vomiting
• Dizziness
• Drowsiness
• Constipation

Precautions

• Use with caution in patients with respiratory depression
• Caution should be exercised in patients with a history of drug abuse

Pregnancy

There is limited data on the safety of noscapine during pregnancy. It should only be used if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether noscapine is excreted in human milk. Caution is advised when administering to nursing mothers.

Storage

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

Formulations

• Oral tablets
• Syrup

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

Noscapine's antitussive effects appear to be primarily mediated by its sigma receptor agonist activity. Evidence for this mechanism is suggested by experimental evidence in rats. Pretreatment with rimcazole, a sigma specific antagonist, causes a dose-dependent reduction in antitussive activity of noscapine. ...EXCEPT FOR ITS ANTITUSSIVE EFFECT, IT HAS NO SIGNIFICANT ACTIONS ON CNS IN DOSES WITHIN THERAPEUTIC RANGE.