QPOL-ANTISEPTIC LIQUID

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

• Antiseptic for skin disinfection
• Hygiene products
• Infection control in healthcare settings

Dosage

Children: Refer to specific product guidelines for appropriate concentrations and application methods.

Adults: Refer to specific product guidelines for appropriate concentrations and application methods.

Mechanism of action

As a phenol antiseptic, chloroxylenol is believed to interact with bacterial cell membranes through its hydroxyl (-OH) groups. This interaction disrupts the membrane integrity, causing cellular contents to leak out. Chloroxylenol further penetrates the bacterial cell, binding to proteins and enzymes, thereby impairing cellular function. At high concentrations, chloroxylenol can coagulate proteins and nucleic acids within the bacterial cells, leading to rapid cell death.

Pharmacodynamics

Chloroxylenol displays bactericidal properties at low concentrations, effectively targeting a wide range of bacteria. Its mechanism of action includes disrupting bacterial cell membranes and interfering with essential cellular processes, which contributes to its effectiveness as an antimicrobial agent in antiseptic and disinfectant applications.

Pharmacokinetics

The pharmacokinetics of chloroxylenol, including absorption, distribution, metabolism, and excretion, are not extensively documented. However, as an agent used primarily for external application, systemic absorption is minimal, and its effects are localized. Further studies may be required to fully elucidate its pharmacokinetic profile.

Pregnancy

There are no adequate and well-controlled studies in pregnant women. Chloroxylenol should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Chloroxylenol is excreted in breast milk. Caution should be exercised when administering to nursing mothers.

Storage

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

Formulations

• Topical solution
• Cream
• Liquid antiseptic

Indications

• Antiseptic for skin disinfection
• Solvent in pharmaceutical formulations
• Cleaning agent in laboratories and healthcare settings

Dosage

Children: For pediatric use, consult specific guidelines in the BNF for Children, as dosing may vary based on age, weight, and clinical circumstances.

Adults: For skin antisepsis, apply isopropyl alcohol topically in a concentration of 70% to the affected area. Dosage may vary based on clinical indication and setting.

Mechanism of action

Isopropyl alcohol works primarily as an antiseptic by denaturing proteins and disrupting cell membranes of bacteria, viruses, and fungi, leading to cell lysis and death. Its efficacy is enhanced by the presence of water, which facilitates the penetration of the alcohol into microbial cells.

Pharmacodynamics

Isopropyl alcohol exhibits a rapid onset of action against a variety of pathogens, including gram-positive and gram-negative bacteria, fungi, and some viruses. Its antimicrobial activity is concentration-dependent, with higher concentrations generally providing a broader spectrum of activity. It is commonly used in concentrations ranging from 60% to 90%, with 70% being optimal for disinfection due to its ability to penetrate the cell wall effectively.

Pharmacokinetics

Isopropyl alcohol is readily absorbed through the skin and mucous membranes. After absorption, it is metabolized primarily in the liver to acetone, which is then further metabolized and excreted, mostly via urine. The elimination half-life of isopropyl alcohol varies but is typically around 2 to 3 hours. Its effects can be influenced by factors such as dosage, route of exposure, and individual metabolic differences.

Pregnancy

Isopropyl alcohol should be used with caution during pregnancy. It is a category C drug, indicating that risk cannot be ruled out.

Breast-feeding

Caution is advised when using isopropyl alcohol during breastfeeding, as it is not known if it is excreted in human milk.

Storage

Isopropyl alcohol should be stored at room temperature, away from heat and flame. Keep the container tightly closed and in a well-ventilated area.

Formulations

• Isopropyl alcohol 70% solution
• Isopropyl alcohol 99% solution

Indications

• Chronic venous insufficiency
• Osteoarthritis
• Hypertension
• Diabetes
• Cardiovascular health
• Antioxidant support

Dosage

Children: Refer to a healthcare professional or product guidelines for pediatric dosing, as safety and efficacy have not been well established in children.

Adults: Refer to the specific product guidelines, as dosages can vary based on the formulation and concentration of the extract.

Mechanism of action

The active compounds in pine bark extract, particularly proanthocyanidins, exert their effects through several mechanisms. They enhance nitric oxide production, which leads to vasodilation and improved blood flow. Additionally, they inhibit the oxidation of low-density lipoprotein (LDL) cholesterol, thus contributing to cardiovascular health. The antioxidant properties help reduce oxidative stress and inflammation by scavenging free radicals and modulating inflammatory pathways.

Pharmacodynamics

Pine bark extract displays a range of pharmacodynamic effects, including vasodilatory, anti-inflammatory, and antioxidant properties. These effects can lead to improved circulation, reduced symptoms of chronic venous insufficiency, and potential benefits in conditions associated with oxidative stress. The anti-inflammatory effects may also contribute to pain relief in osteoarthritis and other inflammatory conditions.

Pharmacokinetics

The pharmacokinetics of pine bark extract are influenced by its route of administration, typically oral. After ingestion, proanthocyanidins are absorbed in the gastrointestinal tract and distributed throughout the body. They undergo metabolic conversion in the liver, with a half-life that can vary based on individual metabolism and formulation. Elimination occurs primarily through urine, with metabolites detectable for several hours post-administration.

Adverse effects

• Allergic reactions
• Skin irritation
• Headache
• Gastrointestinal disturbances

Precautions

• Use with caution in individuals with known allergies to pine products.
• Monitor for allergic reactions in sensitive individuals.

Pregnancy

Pine products should be used with caution during pregnancy. Limited data is available regarding the safety of pine in pregnancy, consult a healthcare provider before use.

Breast-feeding

Caution is advised when using pine products while breastfeeding. Consult a healthcare provider for safety information.

Storage

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

Formulations

• Essential oil
• Extracts
• Topical ointments

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

As a phenol antiseptic, it is believed that the hydroxyl -OH groups of the chloroxylenol molecule binds to certain proteins on the cell membrane of bacteria, and disrupts the membrane so as to allow the contents of the bacterial cell to leak out. This allows chloroxylenol to enter the bacterial cell to bind further with more proteins and enzymes to disable the cell's functioning. At particularly high concentrations of chloroxylenol, the protein and nucleic acid content of targeted bacterial cells become coagulated and cease to function, leading to rapid cell death.

Pharmacodynamics

Chloroxylenol is a substituted phenol which has been widely used for many years as an ingredient of antiseptic and disinfectant products intended for external use. It is known to be bactericidal in low concentration to a wide range of Gram positive and Gram negative bacteria.