Tresor Gentian Violet

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

• Alcohol use disorder
• Anxiety disorders
• Sedation
• Muscle relaxation

Dosage

Children: Refer to the BNF for Children for specific dosing guidelines in paediatric populations.

Adults: Refer to the specific BNF guidelines for dosing related to alcohol use disorder and other indications.

Mechanism of action

Ethyl groups serve primarily as substituents in organic chemistry, influencing the properties and reactivity of the parent molecules. In the context of ethanol, which contains an ethyl group, its mechanism of action involves the enhancement of gamma-aminobutyric acid (GABA) receptor activity, leading to increased inhibitory neurotransmission. This results in its sedative, anxiolytic, and muscle relaxant effects.

Pharmacodynamics

The pharmacodynamics of compounds containing the ethyl group, particularly ethanol, include its effects on the central nervous system, where it acts as a depressant. Ethanol enhances the effects of GABA, resulting in sedation, impaired motor function, and decreased anxiety. It can also affect the dopaminergic pathways, leading to the release of dopamine, which contributes to its reinforcing properties.

Pharmacokinetics

Ethanol is rapidly absorbed from the gastrointestinal tract, with peak blood concentrations typically reached within 30 to 90 minutes after consumption. It is metabolized primarily in the liver by alcohol dehydrogenase and aldehyde dehydrogenase, with a first-order elimination kinetics, typically at a rate of 10 to 15 mL of pure alcohol per hour. Ethanol is also known to exhibit a volume of distribution of approximately 0.5 to 0.7 L/kg in adults.

Indications

• Methemoglobinemia
• Urinary tract infections
• Diagnostic aid in certain surgical procedures
• Potential treatment for other conditions such as malaria

Dosage

Children: Paediatric dosing must be determined based on the specific condition and clinical guidelines. Refer to the BNF for Children for appropriate dosing information.

Adults: Dosage should be guided by the specific clinical condition being treated, considering factors such as severity and patient response. Refer to the relevant clinical guidelines for detailed dosing recommendations.

Mechanism of action

Methylrosanilium functions primarily by acting as a reducing agent. It donates electrons to methemoglobin, reducing it back to hemoglobin, which restores its ability to bind oxygen. This mechanism is particularly beneficial in conditions where methemoglobin levels are elevated.

Pharmacodynamics

The pharmacodynamic properties of methylrosanilium involve its role in reducing methemoglobin, which is formed when iron in hemoglobin is oxidized to the ferric state. The restoration of hemoglobin function leads to improved oxygen delivery to tissues. The drug exhibits a dose-dependent response, where higher concentrations may also exert additional effects such as antimicrobial activity.

Pharmacokinetics

Methylrosanilium is rapidly absorbed when administered intravenously, with peak plasma concentrations occurring shortly after administration. It is distributed throughout the body, including the central nervous system and tissues, and is metabolized primarily in the liver. The elimination half-life of methylrosanilium varies but is typically around 5 to 6 hours. Renal excretion plays a significant role in its clearance, thus dosing adjustments may be necessary in patients with renal impairment.

Contra-indications

• Hypersensitivity to methylrosanilium or any of its components
• Severe renal impairment
• Pregnancy unless clearly needed

Adverse effects

• Hypotension
• Bradycardia
• Nausea
• Vomiting
• Dizziness
• Headache
• Allergic reactions

Interactions

• Antihypertensive agents may enhance the hypotensive effect
• Concurrent use with other vasodilators can increase the risk of adverse effects
• May interact with anesthetic agents

Precautions

• Use with caution in patients with pre-existing cardiovascular diseases
• Monitor blood pressure regularly during treatment
• Caution in patients with a history of hypersensitivity reactions

Pregnancy

Methylrosanilium is not recommended during pregnancy unless the potential benefits outweigh the risks.

Breast-feeding

It is unknown whether methylrosanilium is excreted in human milk. Caution is advised if used during breastfeeding.

Storage

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

Formulations

• Injection solution

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.