TETRANOR 20 %

Indications

• Bacterial infections (e.g. Chlamydia, Rickettsia, Mycoplasma)
• Acne
• Prophylaxis of asymptomatic meningococcal carrier state (not recommended)

Dosage

Adults: For adult patients, the typical dosage of oxytetracycline for susceptible infections is 100 mg twice daily for 5 days. For other conditions, such as acne, the dosage may be 500 mg twice daily, usually for a duration of 6 to 12 weeks, with the possibility of repeating the course intermittently.

Mechanism of action

Oxytetracycline exerts its antibacterial effects by binding to the 30S ribosomal subunit of bacteria, inhibiting the binding of aminoacyl-tRNA to the mRNA-ribosome complex. This action prevents the synthesis of proteins essential for bacterial growth and replication, leading to the bacteriostatic effect of the drug.

Pharmacodynamics

The pharmacodynamics of oxytetracycline involve its ability to inhibit bacterial protein synthesis, which is critical for the growth and reproduction of bacteria. The drug demonstrates a broad spectrum of activity against both Gram-positive and Gram-negative organisms, as well as some atypical pathogens. Its effectiveness can be influenced by the presence of tetracycline resistance mechanisms in certain bacterial strains.

Pharmacokinetics

Oxytetracycline is well absorbed from the gastrointestinal tract, with peak plasma concentrations occurring approximately 1-2 hours after oral administration. It has a relatively long half-life of about 8-10 hours, allowing for twice-daily dosing. The drug is widely distributed in body tissues and fluids, including the liver, kidneys, and lungs, but is less effective in central nervous system infections due to limited penetration. It is primarily excreted via urine, and dosage adjustments may be necessary in patients with renal impairment.

Contra-indications

• Children under 12 years due to deposition in growing bone and teeth, causing staining and occasionally dental hypoplasia

Adverse effects

• Gastrointestinal disturbances
• Photosensitivity
• Dental discoloration
• Hepatotoxicity
• Renal impairment
• Skin reactions including rash and urticaria
• Ataxia
• Hearing impairment
• Colitis
• Systemic lupus erythematosus exacerbation

Interactions

• Antacids and supplements containing calcium, magnesium, or iron may reduce absorption
• Oral contraceptives may be less effective
• Other tetracyclines
• Warfarin (may increase anticoagulant effect)

Precautions

• Use with caution in patients with renal impairment
• Monitor for hepatic toxicity in long-term use
• Patients should be advised to avoid excessive sunlight exposure
• Discontinue if systemic lupus erythematosus develops or worsens

Pregnancy

Oxytetracycline is contraindicated during pregnancy due to potential harm to fetal development, particularly affecting bone and dental health.

Breast-feeding

Use with caution; oxytetracycline is excreted in breast milk and may affect the infant's dental health.

Storage

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

Formulations

• Oxytetracycline 250 mg tablets
• Oxytetracycline oral suspension
• Oxytetracycline oral solution

Indications

• Warts
• Plantar warts
• Verrucas
• Umbilical granulomas

Dosage

Children: Apply twice daily for up to 3 consecutive days. Treatment may be repeated at weekly intervals if necessary for a total of four 3-day treatment courses, under specialist supervision.

Adults: Apply twice daily to the lesion for a maximum of 3 applications. Instructions generally recommend removing dead skin before use by gentle filing and covering with an adhesive dressing after application.

Mechanism of action

Formaldehyde is thought to act via sensory nerve fibers that signal through the trigeminal nerve, reflexively inducing bronchoconstriction through the vagus nerve. It may also disrupt miRNA expression levels within lung cells, representing a novel epigenetic mechanism through which formaldehyde may induce disease. Exposure to formaldehyde has been linked to alterations in gene expression that can contribute to diseases, particularly affecting the respiratory system.

Pharmacodynamics

Formaldehyde exhibits irritant properties, particularly affecting mucosal membranes and respiratory tissues. Its action leads to bronchoconstriction and inflammation upon exposure, indicating significant pharmacological activity as a respiratory irritant. Its potential to induce cellular changes and dysregulation of miRNA expression points to broader implications in disease pathology, particularly in lung tissue.

Pharmacokinetics

Formaldehyde is rapidly absorbed through inhalation and is metabolized primarily in the liver to form formic acid. Its short half-life and high reactivity limit its systemic exposure. The compound is known to form various adducts with proteins and DNA, contributing to its toxicological profile. Excretion is primarily via urine, as formic acid, with minimal excretion of unchanged formaldehyde.

Contra-indications

• Not for application to broken skin
• Not for application to anogenital areas
• Not for application to the face or mucosa

Adverse effects

• Skin irritation
• Rash
• Severe cutaneous adverse reactions
• Methhaemoglobinaemia
• Argyria

Precautions

• Avoid contact with normal skin and open wounds
• Protect surrounding skin with soft paraffin
• May be very irritant to eyes

Pregnancy

Avoid use during pregnancy due to potential harmful effects.

Breast-feeding

Avoid use during breastfeeding due to potential harmful effects.

Storage

Store in a cool, dry place away from light.

Formulations

• Formaldehyde solution 4% (Buffered)
• Formaldehyde liquid 10%

Indications

• Phospholipid biosynthesis disorders
• Neurotransmitter synthesis-related conditions
• Potential use in lipid metabolism abnormalities

Dosage

Children: Refer to the BNF for Children for specific dosing information.

Adults: Refer to the BNF for specific dosing information.

Mechanism of action

Ethanolamine serves as a precursor in the biosynthesis of phospholipids, particularly phosphatidylethanolamine and phosphatidylcholine, which are critical for maintaining cell membrane integrity and functionality. It participates in various metabolic pathways that convert it into other bioactive molecules.

Pharmacodynamics

Ethanolamine's pharmacodynamic properties are largely attributed to its role in phospholipid metabolism. By contributing to the structural integrity of cell membranes, it influences cellular signaling and membrane fluidity, which can affect various physiological responses. Its involvement in neurotransmitter synthesis may also suggest a role in modulating neuronal activity.

Pharmacokinetics

The pharmacokinetics of ethanolamine are not extensively characterized; however, it is generally absorbed when administered and metabolized in the liver. Its metabolites are likely excreted via the kidneys. Specific data regarding half-life, volume of distribution, and clearance are not well-documented.

Pregnancy

Ethanolamine should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether ethanolamine is excreted in human milk. Caution should be exercised when administering to breastfeeding women.

Storage

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

Formulations

• Ethanolamine solution

Indications

• Pain management
• Vaccination
• Antibiotic therapy
• Hormonal therapies
• Anesthesia
• Nutritional support
• Chemotherapy

Dosage

Children: Refer to specific drug guidelines for paediatric dosing, as it requires careful consideration of weight and age.

Adults: Refer to specific drug guidelines for adult dosing, as it varies widely depending on the medication and clinical condition.

Mechanism of action

The mechanism of action of injected drugs varies widely based on the specific medication being administered. Generally, injected drugs enter the bloodstream directly, allowing them to circulate rapidly throughout the body. For instance, antibiotics may work by inhibiting bacterial cell wall synthesis, while analgesics may modulate pain pathways in the central nervous system. Each drug has unique pathways through which it achieves its therapeutic effects.

Pharmacodynamics

Pharmacodynamics refers to the effects of drugs on the body and their mechanisms of action. For injectable medications, effects can be immediate or delayed, depending on the drug's formulation and route of administration. Factors influencing pharmacodynamics include receptor affinity, drug concentration, and the presence of other substances that may enhance or inhibit the drug's effects. For example, some injectable drugs may require specific receptors to exert their effects, while others may have a broader range of action.

Pharmacokinetics

Pharmacokinetics involves the absorption, distribution, metabolism, and excretion (ADME) of injected drugs. After administration, drugs are rapidly absorbed into the bloodstream, leading to quick therapeutic effects. The distribution depends on factors such as blood flow, tissue permeability, and protein binding. Drugs are metabolized primarily in the liver and excreted through the kidneys or bile. The pharmacokinetic profile can vary widely based on the drug's chemical nature, dosage, and individual patient factors.

Pregnancy

Safety during pregnancy depends on the specific injection and its active ingredients. It is essential to consult a healthcare professional for guidance.

Breast-feeding

The safety of injections during breastfeeding varies by the specific medication. It is recommended to seek advice from a healthcare provider.

Storage

Store injections as per manufacturer's guidelines, usually in a cool, dry place away from direct sunlight. Some may require refrigeration.

Indications

• Vision correction
• Phototherapy for skin conditions (e.g., psoriasis, eczema)
• Treatment of seasonal affective disorder (SAD)
• Circadian rhythm disorders
• Wound healing

Dosage

Children: Light therapy for paediatric patients should be approached with caution and always under professional guidance. Specific dosages will depend on the individual treatment protocol and condition being addressed.

Adults: Dosage of light therapy varies based on the condition being treated and should be tailored to individual needs, typically ranging from 15 minutes to 2 hours of exposure per day depending on the specific treatment protocol.

Mechanism of action

Light affects biological systems primarily through phototransduction, which involves the conversion of light into electrical signals within photoreceptor cells in the retina. This process initiates a cascade of biochemical reactions that ultimately lead to visual perception. In addition, specific wavelengths of light can interact with various biological molecules, triggering cellular responses such as the production of vitamin D through skin exposure to UVB radiation.

Pharmacodynamics

The pharmacodynamic effects of light are highly dependent on its wavelength and intensity. Short-wavelength blue light (around 480 nm) is known to influence circadian rhythms by affecting melatonin secretion. In therapeutic settings, light can modulate biological responses, such as promoting wound healing, reducing inflammation, and alleviating symptoms of seasonal affective disorder (SAD) through bright light therapy.

Pharmacokinetics

Light does not undergo traditional pharmacokinetic processes such as absorption, distribution, metabolism, or excretion. Instead, its effects are immediate and localized, depending on the intensity and duration of exposure. The penetration depth of light varies with wavelength; for example, UV light can penetrate the skin and affect deeper tissues, while visible light primarily affects the surface layers.

Pregnancy

There is limited data on the effects of light exposure during pregnancy. However, excessive exposure to bright light can be harmful to both the mother and the developing fetus.

Breast-feeding

Light exposure is generally considered safe while breastfeeding, but excessive exposure should be avoided to prevent potential harm to the infant.

Storage

Light should be properly controlled and managed in environments where it is used, ensuring that exposure levels are safe and effective.

Dosage

Children: Methylpyrrolidone is not indicated for use in paediatric populations, and specific dosing guidelines are not available.

Adults: Methylpyrrolidone is not typically used as a drug for direct therapeutic purposes in adults. Its primary applications are as a solvent in pharmaceutical formulations.

Mechanism of action

Methylpyrrolidone acts primarily as a solvent due to its ability to dissolve a wide range of polar and nonpolar compounds. Its structure allows it to interact with various molecular species, facilitating the dissolution of complex substances. The specific degradation pathway for N-methylpyrrolidone includes its transformation through microbial metabolism, which is a vital aspect of its environmental impact and biodegradability.

Pharmacodynamics

Methylpyrrolidone exhibits low toxicity and is not classified as a carcinogen. Its primary role in pharmacology relates to its use as a solvent rather than direct therapeutic effects. As a solvent, it may influence the bioavailability of drugs by enhancing solubility and stability of active pharmaceutical ingredients.

Pharmacokinetics

Methylpyrrolidone is absorbed through skin and mucous membranes and can be metabolized in the liver. It has a low volatility and its elimination half-life can vary based on exposure levels. The compound is generally excreted via urine. Detailed pharmacokinetic studies in humans are limited.

Pregnancy

There is insufficient data on the use of methylpyrrolidone in pregnant women. Caution is advised.

Breast-feeding

There is limited information regarding the excretion of methylpyrrolidone in human breast milk. Caution is advised.

Storage

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

Mechanism of action

Oxides do not have a single mechanism of action as they are a broad category of compounds. However, in general, metal oxides can exhibit catalytic properties, while non-metal oxides may participate in biochemical reactions by forming acids or bases upon dissolution in water.

Pharmacodynamics

The pharmacodynamics of oxides depend on the specific type of oxide and its interaction with biological systems. For instance, metal oxides may have antimicrobial properties, while certain non-metal oxides can influence metabolic pathways through their acid-base chemistry. The effects vary widely, necessitating specific studies for each oxide's role in therapeutic contexts.

Pharmacokinetics

The pharmacokinetics of oxides are also variable. Many metal oxides are poorly soluble and thus have limited absorption when ingested. Non-metal oxides, such as carbon dioxide, can be readily absorbed and utilized in metabolic processes. The distribution, metabolism, and excretion of oxides depend on their chemical form and the biological system in which they are involved.

Pregnancy

Not applicable as oxide is not a drug but a class of chemical compounds.

Breast-feeding

Not applicable as oxide is not a drug but a class of chemical compounds.

Storage

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

Indications

• Mood disorders
• Anxiety disorders
• Neurotransmitter modulation

Dosage

Children: Refer to the BNF for Children for appropriate paediatric dosing information.

Adults: Refer to the BNF for specific dosing guidance as it may vary based on the condition being treated.

Mechanism of action

Sulfoxylate acts as a modulator of neurotransmitter systems, specifically influencing the activity of monoamines such as serotonin and norepinephrine. It may exert its effects by altering synaptic transmission and enhancing the release of these neurotransmitters, contributing to its therapeutic effects in mood and anxiety disorders.

Pharmacodynamics

The pharmacodynamics of sulfoxylate involve its interaction with receptors and transporters in the central nervous system. By enhancing neurotransmitter availability, it can lead to improved mood and anxiety levels. The precise dose-response relationship and the time course of its effects may vary among individuals, necessitating careful monitoring in clinical use.

Pharmacokinetics

The pharmacokinetics of sulfoxylate are not extensively characterized in the available literature. However, it is expected to be absorbed following administration, with distribution occurring throughout the body, particularly in tissues rich in serotonin and norepinephrine receptors. Metabolism and excretion pathways remain to be fully elucidated, and further studies are required to clarify these aspects.

Pregnancy

Consult with a healthcare professional before use. Limited data available on safety during pregnancy.

Breast-feeding

Consult with a healthcare professional before use. Limited data available on safety during breastfeeding.

Storage

Store in a cool, dry place away from light.

Mechanism of action

Formaldehyde is thought to act via sensory nerve fibers that signal through the trigeminal nerve to reflexively induce bronchoconstriction through the vagus nerve. Exposure to formaldehyde, a known air toxic, is associated with cancer and lung disease. Despite the adverse health effects of formaldehyde, the mechanisms underlying formaldehyde-induced disease remain largely unknown. Research has uncovered microRNAs (miRNAs) as key posttranscriptional regulators of gene expression that may influence cellular disease state. Although studies have compared different miRNA expression patterns between diseased and healthy tissue, this is the first study to examine perturbations in global miRNA levels resulting from formaldehyde exposure. We investigated whether cellular miRNA expression profiles are modified by formaldehyde exposure to test the hypothesis that formaldehyde exposure disrupts miRNA expression levels within lung cells, representing a novel epigenetic mechanism through which formaldehyde may induce disease. Human lung epithelial cells were grown at air-liquid interface and exposed to gaseous formaldehyde at 1 ppm for 4 hr. Small RNAs and protein were collected and analyzed for miRNA expression using microarray analysis and for interleukin (IL-8) protein levels by enzyme-linked immunosorbent assay (ELISA). RESULTS: Gaseous formaldehyde exposure altered the miRNA expression profiles in human lung cells. Specifically, 89 miRNAs were significantly down-regulated in formaldehyde-exposed samples versus controls. Functional and molecular network analysis of the predicted miRNA transcript targets revealed that formaldehyde exposure potentially alters signaling pathways associated with cancer, inflammatory response, and endocrine system regulation. IL-8 release increased in cells exposed to formaldehyde, and results were confirmed by real-time polymerase chain reaction. Formaldehyde alters miRNA patterns that regulate gene expression, potentially leading to the initiation of a variety of diseases. Formaldehyde at high concentrations is a contributor to air pollution. It is also an endogenous metabolic product in cells, and when beyond physiological concentrations, has pathological effects on neurons. Formaldehyde induces mis-folding and aggregation of neuronal tau protein, hippocampal neuronal apoptosis, cognitive impairment and loss of memory functions, as well as excitation of peripheral nociceptive neurons in cancer pain models. Intracellular calcium ([Ca(2+)](i)) is an important intracellular messenger, and plays a key role in many pathological processes. The present study aimed to investigate the effect of formaldehyde on [Ca(2+)](i) and the possible involvement of N-methyl-D-aspartate receptors (NMDARs) and T-type Ca(2+) channels on the cell membrane. METHODS: Using primary cultured hippocampal neurons as a model, changes of [Ca(2+)](i) in the presence of formaldehyde at a low concentration were detected by confocal laser scanning microscopy. Formaldehyde at 1 mmol/L approximately doubled [Ca(2+)](i). (2R)-amino-5-phosphonopentanoate (AP5, 25 umol/L, an NMDAR antagonist) and mibefradil (MIB, 1 umol/L, a T-type Ca(2+) channel blocker), given 5 min after formaldehyde perfusion, each partly inhibited the formaldehyde-induced increase of [Ca(2+)](i), and this inhibitory effect was reinforced by combined application of AP5 and MIB. When applied 3 min before formaldehyde perfusion, AP5 (even at 50 umol/L) did not inhibit the formaldehyde-induced increase of [Ca(2+)](i), but MIB (1 umol/L) significantly inhibited this increase by 70%. These results suggest that formaldehyde at a low concentration increases [Ca(2+)](i) in cultured hippocampal neurons; NMDARs and T-type Ca(2+) channels may be involved in this process. /The purpose of this study was/ to study the role of poly (ADP-ribose) polymerase-l (PARP-1) in formaldehyde-induced DNA damage response in human bronchial epithelial (HBE) cells and to investigate the mechanism of