TRISULPHANOR WATER SOLUBLE POWDER (Each gram contains Sulphaquinoxaline Sodium 200mg/ Sulphadiazine Sodium 90mg/ Sulphadimidine sodium 90mg/ Vitamin K3 5mg/ Vitamin A 15,000iu)

Indications

• Bacterial infections
• Urinary tract infections
• Respiratory tract infections
• Certain types of meningitis
• Toxoplasmosis

Dosage

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

Adults: Refer to BNF for specific dosing guidelines.

Mechanism of action

Sulfadiazine acts as a competitive inhibitor of the bacterial enzyme dihydropteroate synthetase. This enzyme plays a key role in the metabolism of para-aminobenzoic acid (PABA), which is essential for folic acid synthesis in bacteria. By inhibiting this enzyme, sulfadiazine disrupts the production of folic acid, which is vital for bacterial growth and replication.

Pharmacodynamics

Sulfadiazine is classified as a sulfonamide antibiotic, which means it is bacteriostatic and acts by inhibiting bacterial growth. Sulfonamides are effective against a wide spectrum of bacteria, but resistance may develop. The mechanism involves the competitive inhibition of PABA in the folic acid metabolism pathway, which is critical for bacterial survival. While many bacterial strains are sensitive to sulfadiazine, some may show resistance, indicating that sensitivity to one sulfonamide generally implies sensitivity to others.

Pharmacokinetics

Sulfadiazine is well absorbed when taken orally, although parenteral administration is less common due to its alkaline properties that can irritate tissues. The drug distributes widely throughout body tissues and fluids, achieving high concentrations in pleural, peritoneal, synovial, and ocular fluids. Although it is not commonly used for meningitis treatment, it can reach therapeutic levels in the cerebrospinal fluid during meningeal infections. Its antibacterial effectiveness can be reduced in the presence of pus.

Contra-indications

• Hypersensitivity to sulfadiazine or other sulfonamides
• Severe liver or kidney impairment
• Pregnancy near term
• Infants under 2 months of age

Adverse effects

• Nausea
• Vomiting
• Skin rash
• Hematological reactions such as agranulocytosis or thrombocytopenia
• Hypersensitivity reactions including Stevens-Johnson syndrome
• Renal impairment

Interactions

• May enhance the effects of anticoagulants such as warfarin
• May interact with methotrexate, increasing toxicity
• May decrease the efficacy of oral contraceptives
• Probenecid may increase sulfonamide levels and risk of toxicity

Precautions

• Use with caution in patients with G6PD deficiency
• Monitor for signs of blood dyscrasias
• Ensure adequate hydration to prevent crystalluria
• Assess renal function before initiation

Pregnancy

Sulfadiazine should not be used during pregnancy, especially near term, due to potential risks to the fetus.

Breast-feeding

Sulfadiazine is excreted in breast 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

• Tablets
• Oral suspension
• Injectable solution

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

• Bacterial infections
• Skin and soft tissue infections
• Respiratory tract infections
• Urinary tract infections

Dosage

Children: Refer to the BNF for Children for specific dosing recommendations.

Adults: Refer to clinical guidelines or the BNF for specific dosing recommendations.

Mechanism of action

Ulphaquinoxaline exerts its antibacterial effect by inhibiting bacterial DNA synthesis. It interferes with the function of bacterial topoisomerases, enzymes critical for DNA replication and transcription. This inhibition leads to the prevention of bacterial cell division and ultimately results in cell death.

Pharmacodynamics

The pharmacodynamics of ulphaquinoxaline involves its interaction with bacterial cells, where it disrupts the typical processes of DNA replication and repair. Its bactericidal activity is concentration-dependent, meaning higher concentrations of the drug lead to a more significant reduction in bacterial counts. Resistance to ulphaquinoxaline can develop through mutations in target enzymes or through the acquisition of resistance genes.

Pharmacokinetics

Ulphaquinoxaline is absorbed following oral administration, with peak plasma concentrations occurring within a few hours. It is widely distributed throughout body tissues and fluids. The drug is metabolized in the liver and excreted primarily through the kidneys. Its elimination half-life varies based on patient factors but typically ranges from several hours to a day. Dosage adjustments may be necessary in patients with renal impairment.

Pregnancy

No adequate and well-controlled studies have been conducted in pregnant women. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether ulphaquinoxaline is excreted in human milk. Caution should be exercised when administering to a nursing woman.

Storage

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

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

Sulfadiazine is a competitive inhibitor of the bacterial enzyme dihydropteroate synthetase. This enzyme is needed for the proper processing of para-aminobenzoic acid (PABA) which is essential for folic acid synthesis. The inhibited reaction is necessary in these organisms for the synthesis of folic acid.

Pharmacodynamics

Sulfadiazine is a sulfonamide antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of <i>p</i>-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus.

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.