AXAMOL

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

• Dose modification due to adverse drug reactions
• Therapeutic drug monitoring
• Management of drug interactions
• Adjustment for renal or hepatic impairment
• Pediatric dosing adjustments
• Geriatric dosing considerations

Dosage

Children: Refer to the BNF for Children for pediatric dosing adjustments, as they depend on various factors including age, weight, and specific clinical scenarios.

Adults: Refer to the specific drug monograph for detailed dosing information, as adjustments are highly individualized based on patient-specific factors.

Mechanism of action

The mechanism of action for adjustment is not applicable as it is not a specific drug but rather a clinical practice. However, the underlying principle involves tailoring pharmacotherapy to individual patient needs, which may include pharmacokinetic adjustments based on metabolism, clearance rates, and patient adherence.

Pharmacodynamics

Pharmacodynamics in the context of adjustment involves understanding how drugs affect the body and how different variables such as age, weight, kidney and liver function, and concomitant medications can influence the efficacy and safety of a drug regimen. Each adjustment is aimed at optimizing therapeutic outcomes while reducing toxicity.

Pharmacokinetics

Pharmacokinetics in the context of adjustment refers to the study of how the body absorbs, distributes, metabolizes, and excretes medications. Factors such as renal and hepatic function, body mass index, and age play critical roles in determining the appropriate adjustments needed in medication dosing. Understanding these parameters is essential for effective dose adjustment.

Pregnancy

Consult a healthcare professional before use, as the safety of adjustments during pregnancy may vary depending on the specific drug or treatment being adjusted.

Breast-feeding

Consult a healthcare professional before use, as the safety of adjustments during breastfeeding may depend on the specific drug or treatment being adjusted.

Storage

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

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

• Electrolyte replacement
• Volume expansion in hypovolemic patients
• Management of hyponatremia
• Support in intravenous fluid therapy

Dosage

Children: Refer to the BNF for Children for appropriate dosing in paediatric patients, as dosages may vary based on the formulation and clinical condition.

Adults: Refer to specific product information or clinical guidelines for dosage recommendations, as disodium is often part of combination products.

Mechanism of action

Disodium compounds often function by providing sodium ions that are essential for various physiological processes. Sodium ions play a critical role in maintaining osmotic balance, nerve impulse transmission, and muscle contraction. In the context of intravenous solutions, disodium helps to restore electrolyte balance in patients.

Pharmacodynamics

The pharmacodynamics of disodium is primarily related to its role in electrolyte balance and fluid homeostasis. Sodium ions are vital for the function of excitable tissues, including neurons and muscle cells. Changes in sodium levels can affect blood pressure, hydration status, and overall cellular function.

Pharmacokinetics

The pharmacokinetics of disodium compounds depend on their specific formulation and route of administration. When administered intravenously, disodium is rapidly distributed in the extracellular fluid, where it helps to maintain osmotic pressure. Sodium is primarily excreted by the kidneys, and its levels can be influenced by fluid intake, dietary sodium, and renal function.

Pregnancy

Use with caution. Consult a healthcare provider for specific guidance.

Breast-feeding

Use with caution. Consult a healthcare provider for specific guidance.

Storage

Store at room temperature, away from moisture and direct sunlight.

Indications

• Lead poisoning
• Mercury poisoning
• Calcium overload
• Certain diagnostic procedures involving heavy metals

Dosage

Children: Refer to the BNF for Children for appropriate dosing information tailored for paediatric patients.

Adults: Refer to the BNF for specific dosing guidelines based on the condition being treated, considering factors such as the severity of metal poisoning and renal function.

Mechanism of action

Edetate functions by forming stable complexes with divalent and trivalent metal ions, including lead and calcium, through its multiple carboxylate and amine groups. This chelation renders the metals more soluble and promotes their renal excretion, thereby reducing their toxic effects in the body.

Pharmacodynamics

The chelation of metals by edetate decreases the free metal concentration in the bloodstream, which mitigates the toxic effects associated with heavy metal accumulation. The efficacy of edetate in removing metals such as lead has been well documented, and its ability to bind calcium can influence calcium homeostasis in certain clinical scenarios.

Pharmacokinetics

Edetate is administered intravenously, with rapid distribution throughout the extracellular fluid. It is primarily excreted unchanged by the kidneys. The onset of action occurs quickly after administration, and the duration depends on the dose and the patient's renal function. The elimination half-life is approximately 1 hour but may vary based on renal clearance.

Contra-indications

• Hypersensitivity to edetate or any component of the formulation
• Severe renal impairment
• Active bleeding disorders

Adverse effects

• Hypocalcemia
• Nausea
• Vomiting
• Diarrhea
• Abdominal pain
• Headache
• Rash
• Fever

Interactions

• May enhance the effects of anticoagulants
• Concurrent use with calcium supplements may reduce effectiveness
• May interfere with the absorption of certain medications due to changes in gastrointestinal motility

Precautions

• Use with caution in patients with renal impairment
• Monitor electrolyte levels, particularly calcium, during treatment
• Assess the patient's hydration status before administration

Pregnancy

Limited data on the use of edetate in pregnancy. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Caution is advised as it is not known whether edetate is excreted in human milk. Weigh the risks and benefits before use.

Storage

Store in a cool, dry place, protected from light. Do not freeze.

Formulations

• Edetate disodium injection
• Edetate calcium disodium injection

Indications

• Pain management
• Vaccination
• Antibiotic therapy
• Hormonal therapies
• Anesthesia
• Nutritional support
• Chemotherapy

Dosage

Children: Refer to specific drug guidelines for paediatric dosing, as it requires careful consideration of weight and age.

Adults: Refer to specific drug guidelines for adult dosing, as it varies widely depending on the medication and clinical condition.

Mechanism of action

The mechanism of action of injected drugs varies widely based on the specific medication being administered. Generally, injected drugs enter the bloodstream directly, allowing them to circulate rapidly throughout the body. For instance, antibiotics may work by inhibiting bacterial cell wall synthesis, while analgesics may modulate pain pathways in the central nervous system. Each drug has unique pathways through which it achieves its therapeutic effects.

Pharmacodynamics

Pharmacodynamics refers to the effects of drugs on the body and their mechanisms of action. For injectable medications, effects can be immediate or delayed, depending on the drug's formulation and route of administration. Factors influencing pharmacodynamics include receptor affinity, drug concentration, and the presence of other substances that may enhance or inhibit the drug's effects. For example, some injectable drugs may require specific receptors to exert their effects, while others may have a broader range of action.

Pharmacokinetics

Pharmacokinetics involves the absorption, distribution, metabolism, and excretion (ADME) of injected drugs. After administration, drugs are rapidly absorbed into the bloodstream, leading to quick therapeutic effects. The distribution depends on factors such as blood flow, tissue permeability, and protein binding. Drugs are metabolized primarily in the liver and excreted through the kidneys or bile. The pharmacokinetic profile can vary widely based on the drug's chemical nature, dosage, and individual patient factors.

Pregnancy

Safety during pregnancy depends on the specific injection and its active ingredients. It is essential to consult a healthcare professional for guidance.

Breast-feeding

The safety of injections during breastfeeding varies by the specific medication. It is recommended to seek advice from a healthcare provider.

Storage

Store injections as per manufacturer's guidelines, usually in a cool, dry place away from direct sunlight. Some may require refrigeration.

Indications

• Attention Deficit Hyperactivity Disorder (ADHD)
• Narcolepsy
• Chronic fatigue syndrome
• Depression (off-label)

Dosage

Children: Refer to the BNF for Children for appropriate dosing information in paediatric patients.

Adults: Refer to clinical guidelines or prescribing information for specific dosing recommendations, as they vary based on indication and individual patient factors.

Mechanism of action

Make primarily acts as a monoamine reuptake inhibitor, increasing the levels of neurotransmitters such as dopamine, norepinephrine, and serotonin in the synaptic cleft. This action is thought to contribute to its stimulant effects, enhancing mood and alertness.

Pharmacodynamics

The pharmacodynamics of Make involve the modulation of neurotransmitter systems in the brain. By inhibiting the reuptake of monoamines, it enhances synaptic transmission and increases overall neuronal excitability. It may also exhibit effects on peripheral adrenergic receptors, leading to increased heart rate and blood pressure.

Pharmacokinetics

Make is absorbed rapidly after administration, with peak plasma concentrations occurring within 1-2 hours. It is extensively metabolized in the liver, primarily via cytochrome P450 enzymes, and has a half-life of approximately 6-8 hours. Elimination occurs mainly through renal excretion of metabolites.

Pregnancy

The safety of make during pregnancy has not been established. Caution should be exercised.

Breast-feeding

It is unknown whether make is excreted in human milk. Caution should be exercised when administering to nursing mothers.

Storage

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

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.