MiIST EXPECT SED MISTURE (Each 10ml contains Ammonium chloride /Ammonium Bicarbonate / liquonice extract 300mg /200mg/0.5ml

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

• Metabolic acidosis
• Acid-base imbalance
• Urinary alkalinization
• Treatment of certain poisonings
• Cardiac arrest in the context of metabolic acidosis

Dosage

Children: Refer to the BNF for Children for specific pediatric dosages, as they depend on the clinical condition

Adults: Refer to local guidelines and BNF for specific dosing recommendations as they may vary based on clinical condition and severity. General adult dosing for bicarbonate may range from 1 to 2 mEq/kg IV initially, followed by maintenance doses as needed.

Mechanism of action

Bicarbonate acts as a buffer that neutralizes excess acids in the body. It dissociates in solution to produce bicarbonate ions (HCO3-) which can react with hydrogen ions (H+) to form carbonic acid (H2CO3), subsequently leading to the production of carbon dioxide (CO2) and water (H2O). This process helps to raise the pH of the blood and other fluids, counteracting acidosis. Bicarbonate is involved in several metabolic pathways, including the urea cycle and various biosynthetic pathways.

Pharmacodynamics

Bicarbonate's primary pharmacodynamic effect is its ability to buffer hydrogen ions, thus increasing blood pH. This is essential in conditions such as metabolic acidosis, where the body accumulates excess acid. By raising blood pH, bicarbonate can help alleviate symptoms associated with acidemia, such as fatigue, confusion, and shortness of breath. Its effects can also influence the renal and respiratory systems to regulate acid-base homeostasis.

Pharmacokinetics

Bicarbonate is rapidly absorbed from the gastrointestinal tract. It is distributed throughout the body fluids, and its effects can be seen within minutes of administration. The kidneys play a significant role in bicarbonate homeostasis by reabsorbing bicarbonate from urine and excreting hydrogen ions. The elimination half-life can vary, depending on the patient's metabolic state and renal function.

Pregnancy

Use with caution. Consult with a healthcare provider before use.

Breast-feeding

Use with caution. Consult with a healthcare provider before use.

Storage

Store in a cool, dry place away from light.

Indications

• General wellness support
• Anti-inflammatory effects
• Antioxidant activity
• Digestive aid
• Support for immune function

Dosage

Children: Paediatric dosing should be determined based on the specific extract and its intended use. Consultation with a healthcare provider is recommended for accurate dosing.

Adults: Dosage varies widely depending on the specific extract and formulation. It is essential to follow the manufacturer's instructions or consult a healthcare professional for appropriate dosing.

Mechanism of action

The mechanism of action of herbal extracts can vary significantly based on their constituents. Commonly, they exert their effects through multiple pathways including modulation of neurotransmitter systems, interference with inflammatory processes, or direct antioxidant activity. Some extracts may activate certain receptors or inhibit enzymes related to disease processes.

Pharmacodynamics

The pharmacodynamics of extracts is complex due to the presence of multiple active compounds which can have synergistic or antagonistic effects. These compounds may influence cellular signaling pathways, alter gene expression, or modulate immune response. The overall pharmacological profile is determined by the specific composition of the extract, its concentration, and the biological target it interacts with.

Pharmacokinetics

The pharmacokinetics of extracts involves absorption, distribution, metabolism, and excretion of the active compounds. Generally, herbal extracts are absorbed in the gastrointestinal tract, with bioavailability influenced by factors such as formulation, the presence of food, and individual metabolic differences. Compounds may undergo hepatic metabolism, and elimination can occur through urine or feces, depending on their chemical nature.

Pregnancy

Consult a healthcare professional before use, as the safety of the extract during pregnancy has not been established.

Breast-feeding

Consult a healthcare professional before use, as the safety of the extract during breastfeeding has not been established.

Storage

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

Indications

• Insecticide for agricultural use
• Research tool in toxicology

Dosage

Children: Refer to the BNF for Children for specific dosing and administration guidelines.

Adults: Refer to the BNF for specific dosing and administration guidelines.

Mechanism of action

Methyl parathion acts primarily by inhibiting the enzyme acetylcholinesterase, which is essential for the breakdown of the neurotransmitter acetylcholine. Its active metabolite, methyl paraoxon, is a potent inhibitor of both acetylcholinesterase and butyrylcholinesterase. The inhibition of these enzymes results in the accumulation of acetylcholine at synapses, leading to overstimulation of cholinergic receptors and resultant toxic effects.

Pharmacodynamics

The pharmacodynamics of methyl parathion involve its action as a noncompetitive inhibitor of acetylcholinesterase, causing prolonged effects of acetylcholine due to its inability to be hydrolyzed. The resultant cholinergic toxicity can lead to symptoms such as muscle twitching, respiratory distress, and potentially fatal outcomes if not treated promptly. The extent of inhibition is dose-dependent, with significant toxicity occurring after substantial enzyme inhibition.

Pharmacokinetics

Methyl parathion is absorbed through the gastrointestinal tract and can also be absorbed through the skin and respiratory tract. It is metabolized in the liver to form methyl paraoxon, which is responsible for the majority of its toxic effects. The distribution of methyl parathion in body tissues is influenced by its lipophilicity, and it is primarily excreted as metabolites in the urine. The elimination half-life and specific pharmacokinetic parameters can vary based on individual metabolism and exposure levels.

Pregnancy

There are no adequate and well-controlled studies in pregnant women. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether this drug is excreted in human milk. Caution is advised when administering to nursing women.

Storage

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

Formulations

• Liquid formulation

Indications

• Cough and respiratory tract disorders
• Peptic ulcer disease
• Gastroesophageal reflux disease (GERD)
• Adrenal insufficiency
• Inflammatory conditions

Dosage

Children: Refer to the BNF for Children for appropriate dosing.

Adults: Refer to reputable clinical guidelines or pharmacopoeias for appropriate dosing.

Mechanism of action

Glycyrrhizin inhibits the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which typically converts active cortisol to its inactive form, cortisone. This inhibition leads to increased cortisol levels, resulting in mineralocorticoid-like effects such as sodium retention and potassium excretion, which can influence blood pressure and fluid balance. Additionally, liquorice exhibits antioxidant properties and may modulate immune responses.

Pharmacodynamics

Liquorice displays a variety of pharmacological effects including anti-inflammatory, antiviral, and gastroprotective actions. Its anti-inflammatory effects are attributed to the inhibition of pro-inflammatory cytokines and the suppression of immune cell activation. The antiviral properties are primarily linked to its action against viruses such as herpes simplex and hepatitis C. Moreover, liquorice can enhance mucus secretion in the respiratory tract, facilitating the expulsion of phlegm.

Pharmacokinetics

Liquorice is absorbed from the gastrointestinal tract, with glycyrrhizin being the most bioactive compound. Its metabolites can be detected in the plasma, and the elimination half-life is variable, generally between 6 to 12 hours. The metabolism of glycyrrhizin occurs primarily in the liver, and it undergoes phase I and phase II metabolic processes. Excretion mainly occurs through urine, with both active and inactive metabolites present.

Contra-indications

• Hypersensitivity to liquorice or any of its components
• Severe hypertension
• Heart disease
• Kidney disease
• Cirrhosis of the liver

Adverse effects

• Hypertension
• Hypokalemia
• Edema
• Headache
• Fatigue
• Gastrointestinal disturbances
• Muscle weakness
• Arrhythmias

Interactions

• Corticosteroids - may enhance the effects of corticosteroids
• Digoxin - may increase the risk of digoxin toxicity due to hypokalemia
• Diuretics - may reduce effectiveness of potassium-sparing diuretics and increase potassium loss
• Antihypertensives - may counteract the effects of antihypertensive medications

Precautions

• Use with caution in patients with hypertension
• Monitor electrolytes, particularly potassium levels in long-term use
• Avoid excessive consumption, particularly in patients with underlying cardiovascular conditions

Pregnancy

Use during pregnancy is not well studied; consult a healthcare provider before use.

Breast-feeding

Limited information available; consult a healthcare provider before use.

Storage

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

Formulations

• Dried root
• Powder
• Extracts
• Syrups

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

Acute poisoning ... is related to ... inhibiting action on enzyme acetylcholinesterase. Toxic manifestations generally occur only after more than 50% of plasma cholinesterase is inhibited. ... Methyl parathion ... depend on oxidative activation by replacement of thiono-sulfur with oxygen for ... toxicity. Methyl parathion has only a slight inhibitory action on acetylcholinesterase and butyrylcholinesterase, but its active metabolite, methyl paraoxon, is a potent inhibitor of both these enzymes. A study was conducted examining the inhibition of (Ca2+ and Mg2+)-ATPase by parathion (56382) and methyl parathion. Enzyme activity was assessed spectrophotometrically in pig erythrocyte membranes containing calcium2+ (Ca2+) and magnesium2+ and in solubilized membrane preparations incubated with the test agents. The enzyme response to ATP was biphasic. Equations expressing the kinetics of the substrate curves described two classes of the ATP binding active site, one with high affinity and low maximum rate and one with low affinity and high maximum rate. High affinity active sites were stimulated by low ATP concentrations (20 uM), whereas low affinity active sites were stimulated by high ATP levels (2 mM). Parathion and methylparathion dose dependently inhibited enzyme activity; parathion had a greater inhibitory effect than methylparathion. Lineweaver-Burke and Dixon plots indicated noncompetitive inhibition. Parathion and methylparathion induced enzyme inhibition occurred over a range of free calcium ion concentrations (0.5 to 5 mM); the inhibition was significantly greater at lower Ca2+ concentrations (1 to 100 uM) than at higher concentrations. The authors conclude that parathion and methylparathion inhibit ATPase activity by binding to a site on the enzyme rather than through an interaction with associated lipids. For more Mechanism of Action (Complete) data for METHYL PARATHION (6 total), please visit the HSDB record page.