Nilcox Water soluble powder

Indications

• Bacterial infections
• Urinary tract infections
• Respiratory tract infections
• Gastrointestinal infections

Dosage

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

Adults: Refer to the BNF for specific dosing guidelines.

Mechanism of action

Diaveridine exerts its pharmacological effect by inhibiting the enzyme dihydrofolate reductase, which is crucial for the synthesis of tetrahydrofolate. Tetrahydrofolate is necessary for the production of nucleic acids and amino acids, thereby disrupting bacterial DNA synthesis and cell division.

Pharmacodynamics

The bactericidal activity of diaveridine is primarily due to its ability to impede folate metabolism in susceptible bacteria. This action leads to the inhibition of nucleic acid synthesis, ultimately resulting in bacterial cell death. Diaveridine is effective against a range of Gram-negative pathogens, and its efficacy can be influenced by the bacterial strain's sensitivity to the drug.

Pharmacokinetics

Diaveridine is absorbed well after oral administration, with peak plasma concentrations occurring within a few hours. It is distributed widely throughout the body tissues, including the central nervous system. The drug undergoes hepatic metabolism and is excreted primarily via the kidneys. The half-life of diaveridine allows for once or twice daily dosing in most cases, but renal function may necessitate dose adjustments.

Pregnancy

There is insufficient data on the safety of diaveridine in pregnancy. Caution is advised when prescribing to pregnant women.

Breast-feeding

It is not known whether diaveridine is excreted in human breast milk. Caution should be exercised when administering to nursing mothers.

Storage

Store in a well-closed container, at room temperature, away from light and moisture.

Indications

• Bacterial infections of the urinary tract
• Respiratory tract infections
• Certain skin infections
• Other infections caused by susceptible organisms

Dosage

Children: Refer to the BNF for Children for appropriate dosing based on the child's age and weight.

Adults: Refer to the BNF for specific dosing recommendations based on the type and severity of infection.

Mechanism of action

Sulfonamides, including sulphadimidine, inhibit the enzymatic conversion of pteridine and p-aminobenzoic acid (PABA) to dihydropteroic acid by competing with PABA for binding to dihydrofolate synthetase. This inhibition reduces the synthesis of dihydrofolate, which is required for the synthesis of tetrahydrofolic acid (THF). THF is crucial for the synthesis of purines and deoxythymidine monophosphate (dTMP), thereby inhibiting bacterial growth.

Pharmacodynamics

Sulphadimidine is bacteriostatic, meaning it inhibits bacterial growth by preventing the synthesis of dihydrofolic acid. This, in turn, decreases the synthesis of bacterial nucleotides and DNA, effectively limiting the ability of bacteria to reproduce and proliferate within the host.

Pharmacokinetics

Sulphadimidine is well absorbed from the gastrointestinal tract and reaches peak plasma concentrations within a few hours after administration. It is distributed widely throughout body tissues and fluids, including the central nervous system. The drug is metabolized in the liver and excreted primarily via the kidneys in the urine, with a half-life that can vary based on patient factors such as renal function.

Contra-indications

• Hypersensitivity to sulfonamides
• Severe liver or kidney disease
• Porphyria
• Pregnancy at term

Adverse effects

• Rash
• Nausea
• Vomiting
• Diarrhea
• Hematological reactions such as agranulocytosis and aplastic anemia
• Hepatotoxicity
• Renal toxicity

Interactions

• May enhance the anticoagulant effect of warfarin
• May interact with methotrexate, increasing its toxicity
• May decrease the efficacy of oral contraceptives

Precautions

• Use with caution in patients with G6PD deficiency
• Monitor renal function regularly during prolonged therapy
• Use cautiously in patients with asthma or other allergic conditions

Pregnancy

Not recommended in pregnancy, especially during the third trimester due to potential risks to the fetus.

Breast-feeding

Use with caution, as it may pass into breast milk and affect the nursing infant.

Storage

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

Formulations

• Tablets
• Oral suspension

Indications

• Vitamin deficiency syndromes (e.g., scurvy for vitamin C deficiency, rickets for vitamin D deficiency)
• Support for immune function
• Antioxidant support
• Bone health maintenance
• Vision health
• Energy metabolism support

Dosage

Children: Refer to the BNF for Children for specific vitamin dosing guidelines, which depend on age and nutritional requirements.

Adults: Refer to specific vitamin guidelines as dosage varies significantly depending on the type of vitamin and individual needs.

Mechanism of action

Vitamins function primarily as coenzymes or precursors for coenzymes in enzymatic reactions. For instance, B vitamins are involved in energy metabolism, while vitamins A, C, D, E, and K support various physiological functions including vision, antioxidant activity, calcium regulation, and blood clotting. Each vitamin has a unique mechanism of action based on its structure and role in the body.

Pharmacodynamics

Vitamins exert their effects at the cellular level, influencing metabolic pathways, gene expression, and immune responses. For example, vitamin D regulates calcium and phosphate homeostasis, while vitamin A is crucial for vision and immune function. Deficiencies in vitamins can lead to a range of disorders, highlighting their importance in maintaining health.

Pharmacokinetics

The pharmacokinetics of vitamins vary widely. Fat-soluble vitamins (A, D, E, and K) are stored in liver and adipose tissues and can be released into circulation as needed. Water-soluble vitamins (B-complex and C) are not stored and must be consumed regularly, with excess amounts excreted in urine. Absorption rates, half-lives, and distribution can also differ based on the specific vitamin and individual metabolic factors.

Interactions

• tretinoin+vitamin: Severe (increases risk of vitamin toxicity)
• retinoids+vitamin: Severe (increases risk of vitamin toxicity)
• retinoids+vitamin: Moderate (increases risk of toxicity)
• carbamazepine+vitamin: Unknown (decreases effects)
• cobicistat+vitamin: Unknown (increases exposure)
• vitamin D substances+digoxin: Unknown (increases risk of toxicity)
• idelalisib+vitamin: Unknown (increases exposure)
• clarithromycin+vitamin: Unknown (increases exposure)

Pregnancy

Consult healthcare professional before use. Vitamin supplementation during pregnancy should be carefully managed to avoid hypervitaminosis.

Breast-feeding

Consult healthcare professional before use. Some vitamins can pass into breast milk and may affect the infant.

Storage

Store in a cool, dry place, away from direct sunlight. Ensure it is kept out of reach of children.

Formulations

• {'name': 'Vitamin A', 'form': 'Capsule', 'strength': '10000 IU'}
• {'name': 'Vitamin D', 'form': 'Tablet', 'strength': '1000 IU'}
• {'name': 'Vitamin E', 'form': 'Softgel', 'strength': '400 IU'}

Mechanism of action

Sulfonamides inhibit the enzymatic conversion of pteridine and p-aminobenzoic acid (PABA) to dihydropteroic acid by competing with PABA for binding to dihydrofolate synthetase, an intermediate of tetrahydrofolic acid (THF) synthesis. THF is required for the synthesis of purines and dTMP and inhibition of its synthesis inhibits bacterial growth. Pyrimethamine and trimethoprim inhibit dihydrofolate reductase, another step in THF synthesis, and therefore act synergistically with the sulfonamides.

Pharmacodynamics

Sulfamethazine is a sulfonamide drug that inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid (PABA) for binding to dihydropteroate synthetase (dihydrofolate synthetase). Sulfamethazine is bacteriostatic in nature. Inhibition of dihydrofolic acid synthesis decreases the synthesis of bacterial nucleotides and DNA.