FLUBAN Gold

Indications

• Skin disinfection
• Preparation of skin before injections
• Cleansing minor wounds

Dosage

Children: Apply to the skin as required; consult product literature for specific guidance.

Adults: Apply to the skin as required for disinfection.

Mechanism of action

Alcohol exerts its antiseptic effect by denaturing proteins, disrupting cell membranes, and dehydrating microbial cells, leading to cell lysis and death.

Pharmacodynamics

Alcohol has broad-spectrum antimicrobial activity, effective against bacteria, fungi, and viruses. Its efficacy is influenced by concentration, with higher concentrations generally being more effective.

Pharmacokinetics

Alcohol is rapidly absorbed through the skin and mucous membranes. It is metabolized primarily in the liver, with a half-life that varies based on the individual's metabolic rate and the amount consumed.

Contra-indications

• Concomitant use with lithium
• Regular use in neonates
• Patients with severe burns when diathermy has been preceded by application of alcoholic skin disinfectants

Adverse effects

• Eye erythema
• Punctate keratitis
• Cytotoxicity
• Eye discolouration

Interactions

• Increases risk of visual disturbances with antiepileptics
• Increases concentration with methylphenidate
• Increases risk of facial flushing and skin irritation with topical pimecrolimus
• Increases concentration with retinoids
• Increases concentration with acitretin
• Increases risk of facial flushing and skin irritation with topical tacrolimus
• Decreases antidiuretic effect with vasopressin

Precautions

• Avoid regular application to inflamed or broken skin or mucosa
• Avoid broken skin
• Flammable

Pregnancy

Sufficient iodine may be absorbed to affect the fetal thyroid in the second and third trimester.

Breast-feeding

Avoid regular or excessive use.

Storage

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

Formulations

• Betadine 2.5% dry powder spray
• Industrial methylated spirit
• Povidone-Iodine 25 mg per 1 gram

Indications

• Bacterial infections
• Pneumonia
• Meningitis
• Syphilis
• Endocarditis
• Skin and soft tissue infections

Dosage

Children: Paediatric dosing for benzylpenicillin is determined by the child's weight and the severity of the infection. Refer to the BNF for Children for specific dosing guidelines.

Adults: The usual adult dose for benzylpenicillin varies based on the type and severity of the infection. It is generally administered via intramuscular or intravenous routes. For severe infections, doses may range from 1 to 4 million units every 4 to 6 hours.

Mechanism of action

Benzylpenicillin exerts its antibacterial effects by inhibiting the synthesis of bacterial cell walls. It binds to penicillin-binding proteins (PBPs) located inside the bacterial cell wall, disrupting the transpeptidation process, which is crucial for cross-linking peptidoglycan layers. This inhibition leads to cell lysis and death of the bacteria.

Pharmacodynamics

Benzylpenicillin demonstrates time-dependent bactericidal activity, meaning its effectiveness is related to the duration of time the drug concentration remains above the minimum inhibitory concentration (MIC) for the target bacteria. It has a narrow spectrum of activity, primarily targeting Gram-positive cocci and some Gram-negative rods.

Pharmacokinetics

Benzylpenicillin is typically administered parenterally due to poor oral absorption. It is rapidly distributed throughout the body and can penetrate various tissues, including the central nervous system during inflammation. The drug is primarily eliminated by renal excretion, with a half-life of approximately 30 minutes to 1 hour in healthy individuals. Dosage adjustments may be necessary in patients with renal impairment.

Interactions

• leflunomide+benzylpenicillin: Unknown (increases exposure)
• nitisinone+benzylpenicillin: Unknown (increases exposure)
• teriflunomide+benzylpenicillin: Unknown (increases exposure)

Pregnancy

Benzylpenicillin is generally considered safe to use during pregnancy, as it is a penicillin antibiotic and has a long history of use.

Breast-feeding

Benzylpenicillin is excreted in breast milk in small amounts, but it is not expected to have adverse effects on a nursing infant.

Storage

Store in a cool, dry place, protected from light. Reconstituted solutions should be used promptly or stored in a refrigerator and used within a limited time frame.

Formulations

• Benzylpenicillin injection

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
• Zinc toxicity
• Cadmium poisoning
• Iron overload disorders

Dosage

Adults: Refer to the BNF for specific dosing recommendations for adults, as it may vary based on the condition being treated and the severity of metal poisoning.

Mechanism of action

The pharmacologic effects of edetate calcium disodium are due to the formation of chelates with divalent and trivalent metals. A stable chelate forms with any metal that can displace calcium from the molecule, which includes lead, zinc, cadmium, and iron. The excretion of zinc is significantly increased, while the effect on calcium excretion is minimal. The chelation process helps to reduce the toxicity of heavy metals in the body by promoting their urinary excretion.

Pharmacodynamics

Edetate calcium acts as a heavy metal chelating agent, forming stable, water-soluble complexes with metal ions that can be excreted in urine. One gram of edetate calcium can theoretically bind up to 620 mg of lead, though actual urinary excretion rates are lower, with approximately 5 mg of lead excreted per gram of EDTA in lead-poisoned patients. It is relatively ineffective against mercury, gold, or arsenic poisoning but can mobilize and eliminate zinc, cadmium, copper, iron, and manganese.

Pharmacokinetics

After intravenous administration, edetate calcium disodium is rapidly distributed in the blood and has a half-life that can vary based on the patient's condition and the presence of heavy metals. The drug is primarily excreted unchanged in the urine. Calcium levels may be transiently lowered during infusion, but significant mobilization of body calcium stores is usually not observed unless very slow infusions are administered. The effects on metal ion excretion are dose-dependent and vary according to the specific metal involved.

Contra-indications

• Hypersensitivity to edetate calcium disodium or any component of the formulation
• Pre-existing renal impairment
• Calcium deficiency states

Adverse effects

• Hypocalcemia
• Renal impairment
• Gastrointestinal disturbances such as nausea and vomiting
• Headache
• Hypotension
• Electrolyte imbalances

Interactions

• Increased risk of toxicity when used with nephrotoxic agents
• May interfere with the absorption of certain minerals and vitamins
• Should not be mixed with other intravenous drugs due to potential chemical interactions

Precautions

• Monitor renal function during treatment
• Use caution in patients with cardiovascular disease due to potential hypotensive effects
• Evaluate calcium levels periodically in patients receiving prolonged therapy
• Use with caution in patients with a history of seizures

Pregnancy

Limited data available on the use of edetate calcium disodium in pregnant women. Use only if clearly needed.

Breast-feeding

It is not known whether edetate calcium disodium is excreted in human milk. Caution is advised.

Storage

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

Formulations

• Edetate calcium disodium injection

Indications

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

Dosage

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

Adults: Refer to the specific product guidelines for dosing information, as it can vary based on the indication and formulation used.

Mechanism of action

Enrofloxacin exerts its antibacterial effect through the inhibition of bacterial DNA gyrase and topoisomerase IV, which are essential enzymes for DNA replication and transcription. By interfering with these enzymes, enrofloxacin disrupts the normal function of the bacterial cell, leading to cell death.

Pharmacodynamics

Enrofloxacin has a bactericidal effect, meaning it kills bacteria rather than merely inhibiting their growth. Its activity is concentration-dependent, meaning that higher concentrations lead to more significant antibacterial effects. The drug has a broad spectrum of activity against many gram-negative bacteria, including Pseudomonas aeruginosa, as well as some gram-positive organisms.

Pharmacokinetics

Enrofloxacin is well-absorbed after oral administration, with peak plasma concentrations typically achieved within 1 to 2 hours. It is widely distributed throughout the body, including into tissues and fluids, and has good penetration into the central nervous system. The elimination half-life varies but is generally between 4 to 8 hours in humans. Enrofloxacin is primarily metabolized in the liver, and its metabolites, including ciprofloxacin, are also active against bacteria.

Contra-indications

• Hypersensitivity to enrofloxacin or any of its components
• Use in growing animals due to potential effects on cartilage development

Adverse effects

• Gastrointestinal disturbances such as vomiting and diarrhea
• Central nervous system effects including seizures and ataxia
• Tendon rupture or damage, particularly in larger breed dogs
• Possible cartilage damage in young animals

Interactions

• Antacids or products containing aluminum, magnesium, or iron may reduce the absorption of enrofloxacin
• Cationic agents may interfere with its antimicrobial activity
• Concurrent use with other nephrotoxic drugs may increase the risk of renal toxicity

Precautions

• Use with caution in animals with a history of seizures or renal impairment
• Monitor for signs of adverse reactions during therapy
• Not for use in animals with known hypersensitivity to fluoroquinolones

Pregnancy

Safety during pregnancy has not been established, use only if benefits outweigh risks.

Breast-feeding

Safety during lactation has not been fully established, use with caution.

Storage

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

Formulations

• Injectable solution
• Oral tablets
• Oral suspension

Dosage

Children: Refer to specific guidelines for pediatric dosing; consult the BNF for Children for accurate dosage information.

Adults: Refer to specific guidelines for use; dosage may vary based on the context of use.

Mechanism of action

Hydroxide ions act primarily as bases, neutralizing acids to form water and salts. They participate in various biochemical pathways, including selenium metabolism and the degradation of reactive oxygen species. Hydroxide can influence enzyme activity and stability by altering the pH of the environment, thereby affecting metabolic reactions.

Pharmacodynamics

Hydroxide ions can impact biological processes by changing the local pH, which influences enzyme activity, ion transport, and the solubility of other compounds. Their ability to neutralize acids can help regulate physiological pH, contributing to homeostasis in living organisms.

Pharmacokinetics

As an inorganic ion, hydroxide does not undergo traditional pharmacokinetic processes like absorption, distribution, metabolism, or excretion. Instead, it is rapidly equilibrated in biological fluids and participates in acid-base reactions, having immediate effects on the local environment.

Pregnancy

There is limited information regarding the use of hydroxide during pregnancy. Consult a healthcare professional for advice.

Breast-feeding

Limited data is available on the excretion of hydroxide in breast milk. Consult a healthcare professional before use.

Storage

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

Indications

• Food preservation
• Antioxidant in pharmaceuticals
• Treatment of certain conditions related to sulfite sensitivity

Dosage

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

Adults: Refer to specific formulations and clinical guidelines for appropriate dosing, as it varies based on the condition being treated.

Mechanism of action

Metabisulfite acts primarily as a reducing agent, which means it can donate electrons to other compounds, thereby preventing their oxidation. This property is utilized in food preservation and in various chemical reactions. The compound participates in metabolic pathways such as the thiosulfate oxidation and sulfur oxidation pathways, suggesting its role in sulfur metabolism within certain organisms.

Pharmacodynamics

Metabisulfite's pharmacodynamics involve its role as an antioxidant and a preservative. By preventing the oxidation of sensitive compounds, it helps maintain the stability and efficacy of pharmaceuticals and food products. However, it can also induce allergic reactions in sensitive individuals, particularly in those with asthma.

Pharmacokinetics

Metabisulfite is rapidly absorbed when ingested and is metabolized in the body to sulfate, which is then excreted via the kidneys. Its half-life and specific pharmacokinetic parameters can vary based on the route of administration and individual patient factors.

Indications

• Fluid and electrolyte replenishment
• Management of hyponatremia
• Induction of abortion in specific medical circumstances

Dosage

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

Adults: Refer to the BNF for specific dosing guidelines based on clinical context and condition being treated.

Mechanism of action

Sodium and chloride, as major electrolytes in the extracellular fluid, work together to control extracellular volume and blood pressure. Disturbances in sodium concentrations are linked to disorders of water balance. Intra-amniotic instillation of hypertonic sodium chloride may induce uterine contractions, leading to abortion, potentially mediated by prostaglandins released from damaged decidual cells.

Pharmacodynamics

Sodium, the principal cation in extracellular fluid, is critical for regulating water distribution, fluid balance, and osmotic pressure in body fluids. It works in conjunction with chloride and bicarbonate to maintain acid-base equilibrium. Chloride, as the major extracellular anion, mirrors sodium metabolism, and alterations in acid-base balance are reflected in chloride concentrations.

Pharmacokinetics

Sodium and chloride ions are absorbed from the gastrointestinal tract and distributed throughout the body fluids. Their concentration in extracellular fluid is tightly regulated by mechanisms involving renal excretion and hormonal control, primarily through aldosterone. Changes in dietary intake can also influence sodium levels significantly.

Pregnancy

Intra-amniotic instillation of hypertonic sodium chloride is associated with abortion and fetal death. Caution is advised during pregnancy.

Breast-feeding

Sodium is considered safe during breastfeeding as it is an essential electrolyte.

Storage

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

Formulations

• 20% sodium chloride injection

Mechanism of action

Ethanol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate. The sedative effects of ethanol are mediated through binding to GABA receptors and glycine receptors (alpha 1 and alpha 2 subunits). It also inhibits NMDA receptor functioning. In its role as an anti-infective, ethanol acts as an osmolyte or dehydrating agent that disrupts the osmotic balance across cell membranes. ... Ethanol is known to affect a large number of membrane proteins that participate in signaling pathways such as neurotransmitter receptors, enzymes, and ion channels, and there is extensive evidence that ethanol interacts with a variety of neurotransmitters. The major actions of ethanol involve enhancing the inhibitory effects of gamma-aminobutyric acid (GABA) at GABAa receptors and blockade of the N-methyl-D-aspartate (NMDA) subtype of glutamate, an excitatory amine acid (EAA) receptor. Animal studies indicate that the acute effects of ethanol result from competitive inhibition of glycine binding to NMDA receptor and disruption of glutamatergic neurotransmission by inhibiting the response of the NMDA receptor. Persistent glycine antagonism and attenuation of glutamatergic neurotransmission by chronic ethanol exposure results in tolerance to ethanol by enhancing EAA neurotransmission and NMDA receptor upregulation. The latter appears to involve selective increases in NMDA R2B subunit concentrations and other molecular changes in specific brain loci. The abrupt withdrawal of ethanol thus produces a hyperexcitable state that leads to the ethanol withdrawal syndrome and excitotoxic neuronal death. GABA-mediated inhibition, which normally acts to limit excitation, is eliminated during ethanol withdrawal syndrome and further intensifies this excitation. In addition, NMDA receptors function to inhibit the release of dopamine in the nucleus accumbens and mesolimbic structures, which modulate the reinforcing action of addictive xenobiotics such as ethanol. By inhibiting NMDA receptor activity, ethanol could increase dopamine release from the nucleus accumbens and ventral tegmental area and could thus create dependence. Chronic ethanol administration also results in tolerance, dependence, and an ethanol withdrawal syndrome, mediated, in part, by desensitization and or downregulation of GABAa receptors. The development of alcoholic ketoacidosis (AKA) requires that a combination of physical and physiologic events occur. The normal response to starvation and depletion of hepatic glycogen stores is for amino acids to be converted to pyruvate. Pyruvate can serve as a substrate for gluconeogenesis, be converted to acetyl-CoA, which can enter the Krebs cycle or can be utilized in various biosynthetic pathways (eg, fatty acid, ketone bodies, cholesterol, and acetylcholine) ... Ethanol metabolism generates NADH, resulting in an excess of reducing potential. This high redox state favors the conversion of pyruvate to lactate, diverting pyruvate from being a substrate for gluconeogenesis. To compensate for the lack of normal metabolic substrates, the body mobilizes fat from adipose tissue and increased fatty acid metabolism as an alternative source of energy. This response is mediated by a decrease in insulin and an increased secretion of glucagon, catecholamines, growth hormone, and cortisol. Fatty acid metabolism results in the formation of acetyl-CoA and it combines with the excess acetate that is generated from ethanol metabolism to form acetoacetate. Most of the acetoacetate is reduced to beta-hydroxybutyrate due to the excess reducing potential or high redox state of the cell. Volume depletion interferes with the renal elimination of acetoacetate and beta-hydroxybutyrate, and contributes to the acidosis. An elevated lactate concentration may result from shunting from pyruvate or

Pharmacodynamics

Alcohol produces injury to cells by dehydration and precipitation of the cytoplasm or protoplasm. This accounts for its bacteriocidal and antifungal action. When alcohol is injected in close proximity to nerve tissues, it produces neuritis and nerve degeneration (neurolysis). Ninety to 98% of ethanol that enters the body is completely oxidized. Ethanol is also used as a cosolvent to dissolve many insoluble drugs and to serve as a mild sedative in some medicinal formulations. Ethanol also binds to GABA, glycine, NMDA receptors and modulates their effects. Ethanol is also metabolised by the hepatic enzyme alcohol dehydrogenase.

Mechanism of action

The pharmacologic effects of edetate calcium disodium are due to the formation of chelates with divalent and trivalent metals. A stable chelate will form with any metal that has the ability to displace calcium from the molecule, a feature shared by lead, zinc, cadmium, manganese, iron and mercury. The amounts of manganese and iron metabolized are not significant. Copper is not mobilized and mercury is unavailable for chelation because it is too tightly bound to body ligands or it is stored in inaccessible body compartments. The excretion of calcium by the body is not increased following intravenous administration of edetate calcium disodium, but the excretion of zinc is considerably increased. Effects on rat liver glucocorticoid receptor in vitro was studied. At 4 °C, 10 mmole EDTA had a stablizing effect on unbound hepatic glucocorticoid receptors. Apparently, endogenous metal ions are involved in the processes of glucocorticoid-receptor complex stabilization and transformation. Edetate disodium injection forms chelates with the cations of calcium and many divalent and trivalent metals. Because of its affinity for calcium, edetate disodium will produce a lowering of the serum calcium level during intravenous infusion. Slow infusion over a protracted period may cause mobilization of extracirculatory calcium stores. Edetate disodium exerts a negative inotropic effect upon the heart. Edetate disodium likewise forms chelates with other polyvalent metals and produces increases in urinary excretion of magnesium, zinc and other trace elements. It does not form a chelate with potassium but may reduce the serum level and increase urinary loss of potassium.

Pharmacodynamics

Edetate calcium is a heavy metal chelating agent. The calcium in edetate calcium can be displaced by divalent or trivalent metals to form a stable water soluble complex that can be excreted in the urine. In theory, 1 g of edetate calcium can theoretically bind 620 mg of lead, but in reality only about 5 mg per gram is actually excreted into the urine in lead poisoned patients. In addition to chelating lead, edetate calcium also chelates and eliminates zinc from the body. Edetate calcium also binds cadmium, copper, iron and manganese, but to a much lesser extent than either lead or zinc. Edetate calcium is relatively ineffective for use in treating mercury, gold or arsenic poisoning.

Mechanism of action

Sodium and chloride - major electrolytes of the fluid compartment outside of cells (i.e., extracellular) - work together to control extracellular volume and blood pressure. Disturbances in sodium concentrations in the extracellular fluid are associated with disorders of water balance. Intra-amniotic instillation of 20% sodium chloride injection induces abortion and fetal death. Although the mechanism has not been conclusively determined, some studies indicate that the drug's abortifacient activity may be mediated by prostaglandins released from decidual cells damaged by hypertonic solutions of sodium chloride. Hypertonic sodium chloride-induced uterine contractions are usually sufficient to cause evacuation of both the fetus and placenta; however, abortion may be incomplete in 25-40% of patients. /20% injection/

Pharmacodynamics

Sodium, the major cation of the extracellular fluid, functions primarily in the control of water distribution, fluid balance, and osmotic pressure of body fluids. Sodium is also associated with chloride and bicarbonate in the regulation of the acid-base equilibrium of body fluid. Chloride, the major extracellular anion, closely follows the metabolism of sodium, and changes in the acid-base balance of the body are reflected by changes in the chloride concentration.