UNISED 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

• Allergic rhinitis
• Allergic conjunctivitis
• Urticaria
• Insomnia
• Motion sickness
• As an adjunct in anaphylactic reactions

Dosage

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

Adults: Refer to BNF for specific adult dosing guidelines.

Mechanism of action

Diphenhydramine exerts its effects by competitively inhibiting H1 receptors, preventing the action of endogenous histamine. This action leads to decreased symptoms associated with allergic reactions. It also crosses the blood-brain barrier, leading to central nervous system effects, including sedation.

Pharmacodynamics

The primary pharmacodynamic effect of diphenhydramine is its antihistaminic action, which alleviates allergic symptoms. The sedative effects are due to its anticholinergic properties and ability to block H1 receptors in the CNS, leading to drowsiness. It may also have mild antitussive (cough-suppressant) properties.

Pharmacokinetics

Diphenhydramine is rapidly absorbed following oral administration, with peak plasma concentrations typically occurring within 1 to 2 hours. It has a volume of distribution of approximately 4 L/kg, and its metabolism primarily occurs in the liver via cytochrome P450 enzymes. The elimination half-life is approximately 4 to 8 hours in healthy adults, and it is excreted mainly in the urine, with some metabolites excreted in feces.

Contra-indications

• Hypersensitivity to diphenhydramine or any of its components
• Severe asthma attacks
• Narrow-angle glaucoma
• Prostate hypertrophy

Adverse effects

• Drowsiness
• Dizziness
• Dry mouth
• Blurred vision
• Constipation
• Urinary retention

Interactions

• Alcohol may enhance the sedative effect
• CNS depressants (e.g., benzodiazepines, opioids) can increase sedation
• MAO inhibitors may prolong and intensify the anticholinergic effects
• Anticholinergic agents may enhance the effects of diphenhydramine

Precautions

• Use with caution in elderly patients due to increased sensitivity to sedative effects
• Caution in patients with asthma or chronic obstructive pulmonary disease
• Avoid use in patients with a history of seizures
• Exercise caution in those with cardiovascular disease

Pregnancy

Diphenhydramine is classified as a Category B medication. Animal reproduction studies have not shown a risk to the fetus, but there are no adequate studies in pregnant women. It should be used only if clearly needed.

Breast-feeding

Diphenhydramine is excreted in breast milk. Caution is advised when administering to nursing mothers as it may cause sedation in the infant.

Storage

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

Formulations

• Oral tablets
• Oral liquid
• Injectable forms
• Topical creams

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.