Butamed

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

• Treatment of Babesiosis in cattle
• Management of other protozoal infections in veterinary medicine

Dosage

Children: Refer to specific veterinary guidelines for dosing in young animals, as pediatric doses depend on age, weight, and species.

Adults: Refer to specific veterinary guidelines for dosing in adult animals, as dosage may vary based on species and condition.

Mechanism of action

Buparvaquone acts by inhibiting the mitochondrial electron transport chain in protozoa, interfering with their oxidative phosphorylation process. This inhibition leads to a decrease in ATP production, essential for the survival and replication of the protozoa.

Pharmacodynamics

Buparvaquone demonstrates selective toxicity towards protozoa due to its specific interaction with the mitochondrial respiratory chain. The drug exhibits a concentration-dependent effect, with higher concentrations leading to more significant inhibition of protozoal growth. Its efficacy is influenced by the metabolic activity of the target organism.

Pharmacokinetics

Buparvaquone is well-absorbed following oral administration, with peak plasma concentrations typically occurring within a few hours. It has a high volume of distribution and is extensively metabolized in the liver. The primary route of elimination is via feces, with a minor portion excreted in urine. The half-life of buparvaquone is variable, depending on the species and dosage form.

Pregnancy

The safety of buparvaquone in pregnancy has not been established. Caution is advised.

Breast-feeding

It is not known whether buparvaquone 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

• {'name': 'buparvaquone', 'molecular_formula': 'C21H26O3'}

Indications

• Severe infections caused by gram-negative bacteria
• Complicated urinary tract infections
• Bacterial sepsis
• Endocarditis caused by susceptible organisms

Dosage

Children: Dosing in children is also weight-based and varies by indication. Refer to the BNF for Children for specific dosing recommendations.

Adults: Dosage varies significantly based on the infection severity and type, renal function, and the specific bacterial susceptibility. Refer to clinical guidelines or the BNF for precise dosing.

Mechanism of action

Gram works by inhibiting bacterial protein synthesis. It binds to the 30S ribosomal subunit of the bacteria, causing misreading of the mRNA and ultimately preventing the synthesis of essential proteins necessary for bacterial growth and replication.

Pharmacodynamics

The pharmacodynamics of Gram include its bactericidal activity against susceptible bacteria. The drug shows concentration-dependent killing, meaning that higher drug concentrations correlate with greater bactericidal effects. The post-antibiotic effect is noted, where bacterial growth is inhibited even after the drug concentration falls below the minimum inhibitory concentration (MIC).

Pharmacokinetics

Gram is usually administered parenterally (intravenously or intramuscularly), and its absorption can vary based on the route of administration. It is distributed widely in body fluids and tissues, although it does not penetrate well into the central nervous system. The drug is primarily eliminated through the kidneys, and its half-life may be prolonged in patients with renal impairment. Monitoring of drug levels may be necessary to avoid toxicity.

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Abdominal pain
• Allergic reactions
• Rash
• Renal dysfunction

Precautions

• Use with caution in patients with renal impairment
• Monitor renal function during therapy
• Assess for potential allergic reactions

Pregnancy

Use only if the potential benefit justifies the potential risk to the fetus. Consult with a healthcare provider.

Breast-feeding

Use with caution, as it may be excreted in breast milk. Consult with a healthcare provider.

Storage

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

Indications

• Type 2 diabetes mellitus
• Improvement of glycemic control in adults

Dosage

Children: Refer to local guidelines or product information for specific dosing recommendations.

Adults: Refer to local guidelines or product information for specific dosing recommendations.

Mechanism of action

Linagliptin works by inhibiting the enzyme dipeptidyl peptidase-4 (DPP-4). This inhibition increases the levels of incretin hormones, which in turn promote insulin secretion in a glucose-dependent manner and decrease glucagon secretion. The overall effect leads to improved glycemic control without causing significant hypoglycemia.

Pharmacodynamics

Linagliptin's pharmacodynamics involve its ability to enhance the action of incretin hormones, leading to increased insulin secretion from pancreatic beta cells and reduced glucagon secretion from alpha cells. This results in lower blood glucose levels postprandially. Furthermore, linagliptin has a long half-life, allowing for once-daily dosing, which improves patient compliance.

Pharmacokinetics

Linagliptin is well absorbed after oral administration, with peak plasma concentrations occurring approximately 1.5 hours post-dose. It is predominantly eliminated via the bile and feces, with minimal renal elimination, making it a suitable option for patients with renal impairment. The drug has a half-life of approximately 12 hours, allowing for once-daily dosing.

Pregnancy

The safety of linn during pregnancy has not been established. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether linn is excreted in human milk. Caution should be exercised when administering to nursing mothers.

Storage

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

Indications

• Anxiety relief
• Depression
• Insomnia
• Stress reduction
• Antimicrobial therapy
• Anti-inflammatory treatment

Dosage

Children: Consult a qualified healthcare provider for appropriate dosing based on specific conditions and formulations.

Adults: Consult a qualified healthcare provider for appropriate dosing based on specific conditions and formulations.

Mechanism of action

The primary active compounds in jasmine, such as linalool and benzyl acetate, exhibit sedative and anxiolytic properties. These compounds may interact with the GABA-A receptor, enhancing the inhibitory effect of GABA, leading to relaxation and reduced anxiety. Additionally, aromatic compounds in jasmine can influence neurotransmitter levels, including serotonin and dopamine, contributing to mood enhancement.

Pharmacodynamics

Jasmine extracts have been shown to possess anti-inflammatory, antimicrobial, and antispasmodic effects. The sedative properties can assist in alleviating stress and improving sleep quality. Jasmine's aroma has been studied for its potential to reduce anxiety and promote relaxation, influencing the central nervous system's response to stress.

Pharmacokinetics

The pharmacokinetics of jasmine compounds can vary based on the method of extraction and administration. Generally, essential oils are absorbed through the skin or inhaled, entering the bloodstream and exerting systemic effects. Metabolism occurs primarily in the liver, where compounds are transformed into metabolites that are then excreted via urine. However, specific pharmacokinetic parameters for jasmine compounds remain under-researched.

Pregnancy

There is insufficient data on the safety of odorata in pregnancy. Use caution and consult a healthcare provider.

Breast-feeding

Limited information is available regarding the excretion of odorata in breast milk. Consult a healthcare provider before use.

Storage

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

Indications

• Topical drug formulations
• Skin penetration enhancer

Dosage

Children: Refer to the BNF for Children for appropriate formulations and concentrations.

Adults: Refer to specific product guidelines or consult the BNF for appropriate formulations and concentrations.

Mechanism of action

2-Pyrrolidone enhances skin permeation by increasing the diffusivity of polar compounds while decreasing the diffusivity and partitioning of nonpolar compounds through the skin. It acts as a mild accelerant for polar material diffusion, such as methanol, through the human stratum corneum, while inhibiting the transport of nonpolar lipophilic substances.

Pharmacodynamics

Pyrrolidone exhibits unique properties that facilitate the transport of drugs through the skin. Its ability to alter the permeability of the skin barrier allows for enhanced transdermal absorption of active pharmaceutical ingredients, which can lead to improved therapeutic outcomes in topical drug delivery.

Pharmacokinetics

The pharmacokinetics of pyrrolidone involve factors such as its absorption through the skin, distribution within biological tissues, metabolism, and excretion. While specific pharmacokinetic data on 2-pyrrolidone is limited, its role as a skin penetration enhancer suggests that it may exhibit relatively rapid absorption when applied topically. Further studies are needed to elucidate its complete pharmacokinetic profile.

Pregnancy

Safety during pregnancy has not been established. Use only if clearly needed and the benefits outweigh the risks.

Breast-feeding

Not enough data available to determine safety during breastfeeding. Caution is advised.

Storage

Store in a cool, dry place away from light. Keep container tightly closed.

Indications

• Muscle spasticity
• Anxiety disorders
• Sedation prior to surgical procedures
• Management of muscle pain or discomfort

Dosage

Children: Refer to the BNF for Children for specific dosing recommendations in paediatric patients. Doses are typically adjusted according to age and weight.

Adults: Refer to relevant clinical guidelines or the BNF for specific dosing information. Dosage may vary based on condition being treated and patient response.

Mechanism of action

Span acts as a positive allosteric modulator of the GABA-A receptor. By binding to this receptor, Span enhances the inhibitory effect of gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system. This leads to increased neuronal hyperpolarization, resulting in muscle relaxation and sedation.

Pharmacodynamics

The pharmacodynamic properties of Span are characterized by its ability to induce muscle relaxation, sedation, and anxiolytic effects. The onset of action may vary depending on the route of administration, with intravenous administration producing effects more rapidly than oral forms. The therapeutic effects are generally dose-dependent, with higher doses yielding more pronounced muscle relaxant and sedative effects.

Pharmacokinetics

Span is well-absorbed when administered orally, with peak plasma concentrations typically occurring within 1 to 3 hours. It is metabolized primarily in the liver via cytochrome P450 enzymes, particularly CYP3A4. The elimination half-life can vary significantly among individuals, often ranging from 6 to 12 hours, depending on dosing and individual metabolism. The drug is excreted mainly in urine as metabolites.

Pregnancy

Use during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Use with caution, as it is not known if this drug is excreted in human milk.

Storage

Store at room temperature, away from moisture and heat.

Indications

• Respiratory tract infections
• Inflammatory skin conditions
• Cough and cold symptoms
• Diuretic needs
• Allergic rhinitis

Dosage

Children: Paediatric dosing for Viola is also not established and should be approached with caution. Consultation with a healthcare provider is recommended for appropriate herbal dosing in children.

Adults: Dosage for Viola is not standardized and may vary based on the form of preparation and specific indication. It is advised to refer to professional herbal medicine guidelines for appropriate dosing.

Mechanism of action

The exact mechanism of action of Viola species is not fully elucidated. However, it is believed that the active compounds may exert their effects through modulation of inflammatory pathways, antioxidant activity, and possibly influencing mucosal secretions in the respiratory tract.

Pharmacodynamics

Viola exhibits various pharmacological activities attributed to its phytochemical constituents, including flavonoids, saponins, and tannins. These compounds are believed to possess anti-inflammatory, antimicrobial, and antioxidant properties, contributing to the plant's therapeutic effects. The anti-inflammatory action may be beneficial in conditions such as respiratory tract infections and skin inflammations.

Pharmacokinetics

The pharmacokinetics of Viola species are not well-documented in the scientific literature. However, when used in traditional herbal preparations, it is presumed that the active constituents are absorbed in the gastrointestinal tract, metabolized by the liver, and excreted via the kidneys. The bioavailability and half-life of specific compounds can vary based on preparation methods and individual patient factors.

Pregnancy

Consult a healthcare provider for safety and potential risks during pregnancy, as specific data may be limited.

Breast-feeding

Consult a healthcare provider, as the effects during breastfeeding are not well established.

Storage

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

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 MECHANISMS OF SKIN PENETRATION ENHANCERS WERE INVESTIGATED BY MEASURING STEADY-STATE FLUXES IN VITRO FOR MODEL COMPOUNDS, METHANOL, OCTANOL & CAFFEINE. 2-PYRROLIDONE ENHANCED THEIR PERMEATION THROUGH THE POLAR ROUTE OF THE SKIN BY INCREASING THE DIFFUSIVITY & DECREASED PASSAGE THROUGH THE NONPOLAR ROUTE BY DECREASING DIFFUSIVITY & PARTITIONING. TRYPSINIZED, ABDOMINAL STRATUM CORNEUM ABSORBED 1-4 TIMES ITS WT OF PRIMARY ALCOHOLIC VEHICLE FROM SOLUTIONS OF 0-80% WT 2-PYRROLIDONE IN WATER; ABOUT 2 SEPARATION PARTITION COEFFICIENTS OPERATED. CALCULATIONS OF HM VALUES FOR THE PARTITIONS INDICATED THAT 2-PYRROLIDONE IS PROBABLY NOT A PENETRATION ACCELERANT FOR C1-C8 PRIMARY ALCOHOLS. FOR THE SIMPLE NONELECTROLYTES TESTED, & UNDER IDEALIZED IN VITRO STEADY STATE CONDITIONS, 2-PYRROLIDONE ACTED AS A MILD ACCELERANT FOR POLAR MATERIAL (METHANOL) DIFFUSION THROUGH HUMAN STRATUM CORNEUM, BUT INHIBITED NONPOLAR, LIPOPHILIC (OCTANOL) TRANSPORT.