Injectal

Indications

• Prevention of postoperative nausea and vomiting
• Treatment of nausea and vomiting
• Premedication for surgical procedures

Dosage

Children: Refer to the BNF for Children for age-appropriate dosing guidelines.

Adults: Refer to the BNF for specific dosing recommendations based on the clinical context and patient condition.

Mechanism of action

Droperidol primarily acts as an antagonist at dopamine D2 receptors in the central nervous system. This blockade of dopamine receptors leads to a decrease in nausea and vomiting, as dopamine is a key neurotransmitter involved in these processes. Furthermore, droperidol may also have some affinity for other receptor types, including adrenergic and serotonin receptors, contributing to its sedative and antiemetic effects.

Pharmacodynamics

The pharmacodynamic profile of droperidol includes its ability to reduce the incidence of nausea and vomiting through central action. It can also produce sedation and anxiolytic effects, making it useful in preoperative settings. The onset of action is typically rapid, with effects observed shortly after administration. Droperidol has a dose-dependent relationship, where higher doses may lead to increased sedation and potential extrapyramidal side effects due to its dopamine antagonism.

Pharmacokinetics

Droperidol is well-absorbed after parenteral administration, with peak plasma concentrations occurring within 30 minutes to 1 hour. It is metabolized in the liver, primarily via cytochrome P450 enzymes, and has a relatively short half-life, generally ranging from 1 to 3 hours. Droperidol is excreted mainly in urine as metabolites, with less than 1% of the dose excreted unchanged. The drug's pharmacokinetic profile can be influenced by factors such as age, liver function, and concurrent medications.

Interactions

• droperidol + dopaminereceptor agonists: Severe (decreases effects)
• droperidol + levodopa: Unknown (decreases effects)

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

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.