Prazitel

Indications

• Dry eye conditions
• Tear deficiency
• Keratoconjunctivitis sicca

Dosage

Children: Apply as required, typically in the form of eye drops.

Adults: Apply as required, typically in the form of eye drops.

Mechanism of action

Hypromellose acts by forming a viscous gel upon contact with the ocular surface, which helps to retain moisture and protect against irritants. This gel-like property enhances the stability of the tear film and reduces evaporation, thereby alleviating symptoms associated with dry eye conditions.

Pharmacodynamics

The pharmacodynamic effects of hypromellose are primarily related to its ability to mimic natural tears, providing lubrication to the ocular surface. This lubrication reduces friction during blinking and maintains corneal hydration, which is critical for ocular comfort and health. Its high viscosity also contributes to prolonged retention time on the eye surface.

Pharmacokinetics

Hypromellose is administered topically as eye drops and is not significantly absorbed systemically. The retention time of hypromellose on the ocular surface is enhanced due to its viscosity, allowing for extended relief of dry eye symptoms. The elimination of hypromellose occurs primarily through drainage from the eye and dilution by the natural tear fluid.

Adverse effects

• Temporary visual disturbance
• Eye irritation

Precautions

• Should not be used during contact lens wear
• Use with caution in patients with known hypersensitivity to any component of the formulation

Pregnancy

Hypromellose is generally considered safe for use during pregnancy. However, it should be used only if clearly needed and after consulting a healthcare provider.

Breast-feeding

Hypromellose is unlikely to affect breastfed infants when used as directed, but consultation with a healthcare provider is advisable.

Storage

Store in a cool, dry place away from direct sunlight. Once opened, use within a specified period as indicated on the packaging.

Formulations

• {'name': 'Teardew', 'concentration': '0.3%', 'form': 'eye drops', 'volume': '10 ml'}
• {'name': 'Xailin Hydrate', 'concentration': '0.3%', 'form': 'eye drops', 'volume': '10 ml'}
• {'name': 'AacuLose', 'concentration': '0.3%', 'form': 'eye drops', 'volume': '10 ml'}
• {'name': 'Artelac', 'concentration': '0.32%', 'form': 'eye drops', 'volume': '10 ml'}
• {'name': 'Lacrilube', 'concentration': '2 mg/g', 'form': 'eye ointment', 'volume': '3.5 g'}
• {'name': 'Celluvisc', 'concentration': '1%', 'form': 'eye drops', 'volume': '0.4 ml unit dose'}

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

• Schistosomiasis caused by Schistosoma mansoni
• Schistosomiasis caused by Schistosoma japonicum
• Tapeworm infections, including Taenia solium and Hymenolepis nana

Mechanism of action

Praziquantel is hypothesized to target the β subunits of voltage-gated Ca2+ channels in parasites such as Schistosoma mansoni and Schistosoma japonicum. This action leads to increased calcium influx, causing rapid contraction and paralysis of the worms. The drug also induces tegumental disintegration and vacuolization in schistosomes, significantly affecting adult worms more than juveniles. Secondary effects include inhibition of glucose uptake and depletion of glycogen levels.

Pharmacodynamics

Praziquantel exhibits a rapid onset of action against trematodes and cestodes, causing significant changes in the permeability of the cell membrane of the parasites. This results in muscle contraction, tegumental damage, and eventual death of the worms. It selectively targets schistosomes and is ineffective against nematodes. The drug's efficacy is notably reduced against juvenile schistosomes and may diminish after a few weeks of treatment.

Pharmacokinetics

Praziquantel is well absorbed from the gastrointestinal tract, with peak plasma concentrations occurring within 1-3 hours post-administration. It undergoes extensive hepatic metabolism, primarily by CYP450 enzymes, and has a half-life of approximately 1-3 hours. The drug is excreted mainly in urine as metabolites, with a small fraction excreted unchanged. The pharmacokinetics can be affected by co-administration with certain other drugs that alter its metabolism.

Adverse effects

• dizziness
• hepatitis
• neutropenia
• seizure
• severe cutaneous adverse reactions

Interactions

• mitotane+praziquantel: Severe (decreases exposure)
• rifampicin+praziquantel: Severe (decreases exposure)
• chloroquine+praziquantel: Moderate (decreases exposure)
• cobicistat+praziquantel: Unknown (increases exposure)
• dexamethasone+praziquantel: Unknown (decreases exposure)
• grapefruit juice+praziquantel: Unknown (increases exposure)
• cimetidine+praziquantel: Unknown (increases exposure)
• idelalisib+praziquantel: Unknown (increases exposure)

Pregnancy

Manufacturer advises avoiding use due to toxicity observed in animal studies.

Breast-feeding

Amount present in milk is too small to be harmful; however, the manufacturer advises avoiding use.

Storage

Store in a cool, dry place away from light.

Formulations

• tablets
• oral suspension

Indications

• Used as an excipient in various pharmaceutical formulations
• Facilitates controlled release of active ingredients
• Improves stability and texture of drug products

Dosage

Children: Refer to specific formulation guidelines, as carnauba is used as an excipient rather than a drug with a defined dosage.

Adults: Refer to specific formulation guidelines, as carnauba is used as an excipient rather than a drug with a defined dosage.

Mechanism of action

Carnauba wax functions primarily as an excipient in drug formulations. It acts as a matrix-forming agent that can alter the release rate of active pharmaceutical ingredients. The wax forms a hydrophobic barrier that can modulate the dissolution rate of drugs, thereby influencing their bioavailability.

Pharmacodynamics

Carnauba wax does not have a pharmacological effect in the traditional sense, as it is not a therapeutic agent. Instead, its role is to enhance the physical properties of drug formulations, providing stability and modifying release profiles. It is well-tolerated and considered safe for use in pharmaceutical applications.

Pharmacokinetics

As an excipient, carnauba wax is not absorbed into the systemic circulation in significant amounts. It passes through the gastrointestinal tract largely unchanged. Due to its inert nature, it does not exhibit pharmacokinetic parameters like absorption, distribution, metabolism, or excretion that are typically associated with active drugs.

Pregnancy

Carnuba wax is generally considered safe for use in food and cosmetics during pregnancy. However, it is always advisable for pregnant individuals to consult healthcare professionals before using any product containing carnauba wax.

Breast-feeding

Carnauba wax is considered safe during breastfeeding when used in food and cosmetics, but consulting a healthcare professional is recommended for personalized advice.

Storage

Store in a cool, dry place away from direct sunlight. Keep container tightly closed to prevent contamination.

Formulations

• Carnauba wax flakes
• Carnauba wax powder
• Carnauba wax emulsions

Indications

• Constipation
• Dietary fiber supplementation
• Irritable bowel syndrome
• Diverticular disease
• Weight management

Dosage

Children: Refer to appropriate guidelines for specific dosage; generally taken with adequate fluid intake.

Adults: Refer to appropriate guidelines for specific dosage; generally taken with adequate fluid intake.

Mechanism of action

Cellulose acts primarily as a bulk-forming laxative. It absorbs water in the intestines, which increases stool bulk and stimulates peristalsis, thus facilitating bowel movements. Additionally, cellulose is not digestible by human enzymes, leading to fermentation by gut bacteria, which may enhance gut health and alter gut microbiota composition.

Pharmacodynamics

Cellulose increases stool weight and frequency of bowel movements. It works by retaining water in the intestines, leading to softer stools and improved passage through the gastrointestinal tract. The bulking effect of cellulose can help alleviate constipation and promote overall digestive health. It may also play a role in cholesterol reduction and glycemic control through its effects on digestion and absorption of nutrients.

Pharmacokinetics

Cellulose is not absorbed into the bloodstream due to its indigestible nature. Instead, it passes through the gastrointestinal tract, where it adds bulk to the stool. Its fermentation by colonic bacteria produces short-chain fatty acids, which may have beneficial effects on colon health. The onset of action for cellulose as a laxative can vary but is generally within 24 to 72 hours after ingestion.

Adverse effects

• Bloating
• Flatulence
• Diarrhea
• Abdominal discomfort

Precautions

• Use with caution in patients with a history of gastrointestinal disorders.
• Monitor for potential allergic reactions in sensitive individuals.

Pregnancy

Cellulose is generally considered safe during pregnancy as it is a non-toxic, indigestible fiber.

Breast-feeding

Cellulose is also considered safe during breastfeeding; it is excreted in breast milk in negligible amounts.

Storage

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

Formulations

• Powder
• Capsules
• Tablets
• Granules

Dosage

Children: Chloroform is not indicated for pediatric use due to safety concerns and potential for toxicity. Refer to specific clinical guidelines for any related interventions or alternative agents.

Adults: Chloroform is not commonly used in clinical practice today and specific dosing recommendations should be referred to in relevant clinical guidelines or literature. It is important to note that due to its toxicity, chloroform usage is highly restricted.

Mechanism of action

Chloroform undergoes bioactivation primarily through covalent binding to lipids and proteins, particularly under anaerobic conditions with the presence of NADPH. This process is linked to the inhibition of cytochrome P450 and related mono-oxygenases, with biotransformation being mediated by phenobarbital-inducible P450 isozymes. The resultant oxidation products impair the monooxygenase system, potentially leading to protein aggregation.

Pharmacodynamics

Chloroform has a depressant effect on the central nervous system, leading to sedation and anesthesia at sufficient exposure levels. Its effect on cytochrome P450 enzymes suggests a mechanism that can alter drug metabolism and pharmacokinetics of concurrently administered medications, potentially leading to toxic accumulation or therapeutic failure.

Pharmacokinetics

Chloroform is rapidly absorbed through inhalation and dermal exposure, with distribution throughout the body, including the liver and brain. It is metabolized primarily in the liver via the cytochrome P450 system, leading to the formation of reactive intermediates. Chloroform and its metabolites are eliminated through exhalation and renal excretion, but the potential for accumulation and toxicity remains a concern.

Pregnancy

Chloroform is not recommended for use during pregnancy due to potential risks to fetal development.

Breast-feeding

Chloroform is not recommended during breastfeeding as it may be excreted in breast milk and could pose risks to the infant.

Storage

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

Mechanism of action

Dichloromethane induces mammary adenomas in rats through an indirect mechanism involving hyperprolactinaemia, resulting in benign neoplasms. It does not bind to DNA in various tissues, suggesting that its carcinogenic effects are likely mediated through metabolic pathways in the liver. In mice, DCM acts as a hepatic and pulmonary carcinogen, mediated by interaction with DNA through a glutathione (GSH) conjugate produced by the enzyme glutathione S-transferase T1-1 (GST T1-1).

Pharmacodynamics

Dichloromethane exhibits carcinogenic properties, particularly evident in animal studies where exposure leads to liver and lung tumors. The incidence of tumors varies by species, with higher susceptibility observed in mice due to differences in glutathione transferase activity. Its effects on humans are still uncertain, necessitating caution in its handling and use due to potential health risks.

Pharmacokinetics

Dichloromethane is rapidly absorbed through inhalation and dermal exposure, with peak blood concentrations occurring shortly after exposure. It undergoes extensive hepatic metabolism primarily via cytochrome P450 enzymes, leading to the formation of reactive metabolites. The elimination half-life is relatively short, with excretion occurring mainly through the lungs and urine.

Pregnancy

Dichloromethane should be avoided during pregnancy due to its potential carcinogenic effects and lack of safety data in pregnant women.

Breast-feeding

It is not known whether dichloromethane is excreted in human milk, thus it should be used with caution in breastfeeding mothers.

Storage

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

Dosage

Children: Refer to BNF for Children for appropriate dosing guidelines, as specific therapeutic doses are not applicable for butane.

Adults: Refer to BNF for appropriate dosing guidelines, as specific therapeutic doses are not applicable for butane.

Mechanism of action

Butane acts primarily as a central nervous system depressant when inhaled, leading to hypoxia and potential cardiac complications. The inhalation of butane can result in a range of toxic effects, including asphyxia due to displacement of oxygen and direct toxic effects on cardiac tissues, which can lead to arrhythmias and myocardial damage.

Pharmacodynamics

The pharmacodynamic properties of butane involve its effects on the central nervous system, where it enhances inhibitory neurotransmission. This can lead to sedation and a decreased level of consciousness. Additionally, butane can cause cardiovascular effects, including changes in heart rhythm and potential myocardial ischemia due to oxygen deprivation.

Pharmacokinetics

Butane is rapidly absorbed through the lungs upon inhalation. Its distribution throughout the body is quick due to its lipophilic characteristics, allowing it to cross cell membranes efficiently. Metabolism of butane occurs primarily in the liver, although specific metabolic pathways are not extensively characterized. The elimination half-life is variable and dependent on the duration and intensity of exposure.

Contra-indications

• Hypersensitivity to butane or any of its components
• Severe respiratory insufficiency
• Acute or chronic pulmonary disease

Adverse effects

• Asphyxia
• Cardiac arrhythmias
• CNS depression
• Dizziness
• Headache
• Nausea
• Vomiting
• Confusion
• Loss of consciousness

Interactions

• May potentiate the effects of other CNS depressants
• Use with caution in patients receiving medications that affect cardiac rhythm

Precautions

• Use in well-ventilated areas to reduce inhalation risk
• Monitor patients for signs of respiratory distress
• Avoid use in individuals with a history of substance abuse

Pregnancy

There are no adequate and well-controlled studies in pregnant women. Use only if clearly needed and the potential benefits justify the potential risks.

Breast-feeding

It is not known whether butane is excreted in human milk. Caution should be exercised when administered to a nursing woman.

Storage

Store in a cool, well-ventilated area away from heat and flames. Keep container tightly closed.

Formulations

• Aerosol propellant
• Lighter refills

Indications

• Monitoring respiratory function
• Assessment of metabolic status
• Management of respiratory acidosis
• Management of respiratory alkalosis

Dosage

Children: Dosing for interventions related to carbon dioxide levels in pediatric patients should be guided by clinical protocols and the BNF for Children.

Adults: Dosing for interventions related to carbon dioxide levels is typically based on clinical assessment and individual patient needs. Refer to clinical guidelines for specific scenarios.

Mechanism of action

Carbon dioxide acts primarily as a signaling molecule in the body, influencing respiratory drive and blood pH. It is produced during cellular respiration and is a critical component of the bicarbonate buffering system, which helps maintain acid-base homeostasis. Elevated levels of CO2 in the blood stimulate ventilation in the lungs, increasing the rate of gas exchange and facilitating the removal of excess CO2.

Pharmacodynamics

The pharmacodynamic effects of dioxides, particularly carbon dioxide, are closely related to its concentration in the blood. As CO2 levels increase, it leads to respiratory acidosis, which can stimulate the respiratory centers in the brain to increase ventilation. Conversely, low levels of CO2 can cause respiratory alkalosis, potentially leading to decreased respiratory drive. CO2 also plays a role in vasodilation and can affect blood flow and pressure through its influence on smooth muscle tone.

Pharmacokinetics

Carbon dioxide is produced endogenously during metabolic processes and is transported in the bloodstream primarily in three forms: dissolved in plasma, as bicarbonate ions (HCO3-), and bound to hemoglobin. The half-life of CO2 in the bloodstream is very short due to its rapid exchange with alveolar gas in the lungs. The elimination of CO2 occurs through exhalation, making it a dynamic component of respiratory physiology.

Pregnancy

Data on the effects of dioxide during pregnancy are limited. Caution is advised due to potential risks associated with exposure.

Breast-feeding

Limited data are available regarding the excretion of dioxide in human milk. Caution is recommended.

Storage

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

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.

Dosage

Children: Refer to specific clinical guidelines for dosing in children, as no standard paediatric dosage is specified in the provided resources.

Adults: Refer to specific clinical guidelines for dosing, as no standard adult dosage is specified in the provided resources.

Mechanism of action

Ethylene glycol toxicity results from its metabolism to glycolic acid and other toxic metabolites. Glycolate accumulates in the body and is eliminated more slowly than ethylene glycol itself. The renal excretion of both compounds plays a crucial role in their elimination, accounting for a significant portion of the administered dose.

Pharmacodynamics

The pharmacodynamics of glycolate are closely tied to its role as a metabolite of ethylene glycol. Its accumulation can lead to metabolic acidosis, although minimal clinical effects have been observed at low doses. The relationship between glycolate and ethylene glycol indicates that glycolate may contribute to the overall toxic effects of ethylene glycol ingestion.

Pharmacokinetics

The pharmacokinetics of glycolate indicate that it reaches peak plasma levels between 4-6 hours after the administration of ethylene glycol. The elimination half-life of ethylene glycol is approximately 1.7 hours in rats and 3.4 hours in dogs. Glycolate is predominantly eliminated through renal excretion, with about 5% of the dose being excreted unchanged.

Pregnancy

There is limited data on the safety of glycolate in pregnancy. Caution is advised.

Breast-feeding

Data on the excretion of glycolate in human milk is not available. Caution is advised.

Storage

Store at room temperature, away from light and moisture.

Dosage

Children: Refer to specific pediatric dosing guidelines based on the identified drug, as 'hard' does not provide sufficient information.

Adults: Refer to specific drug information for dosing guidelines, as 'hard' does not specify a particular medication.

Mechanism of action

The mechanism of action for drugs termed 'hard' must be specified for accurate information, as this phrase does not designate a specific compound. Mechanisms may involve receptor interaction, enzyme inhibition, or modulation of biochemical pathways, depending on the drug in question. For example, opioid analgesics work primarily by binding to mu-opioid receptors in the central nervous system, leading to analgesic effects.

Pharmacodynamics

Pharmacodynamics refers to the effects of a drug on the body and its mechanisms of action. The pharmacodynamics of any drug classified as 'hard' would depend on its specific pharmacological profile, including its efficacy, potency, and the nature of its therapeutic effects. For instance, in the case of opioids, pharmacodynamic effects include pain relief, sedation, and potential respiratory depression.

Pharmacokinetics

Pharmacokinetics involves the absorption, distribution, metabolism, and excretion (ADME) of a drug. The pharmacokinetics of a substance termed 'hard' would vary significantly based on the specific drug. For many medications, absorption may occur via oral or parenteral routes, distribution may involve binding to plasma proteins, metabolism may occur in the liver, and excretion is typically renal. Each of these parameters is critical for understanding the drug's action and potential side effects.

Pregnancy

Consult a healthcare professional before use, as safety has not been established.

Breast-feeding

Consult a healthcare professional before use, as safety has not been established.

Storage

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

Indications

• Cleansing agent in topical formulations
• Emulsifying agent in cosmetic products
• Foaming agent in shampoos and body washes

Dosage

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

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

Mechanism of action

Lauryl sulfate functions as an anionic surfactant. It reduces the surface tension between different substances, allowing for better spreading and wetting. In the context of cleansing, it facilitates the removal of dirt and oils from the skin and hair by emulsifying these substances, thus making them easier to rinse away with water.

Pharmacodynamics

As a surfactant, lauryl sulfate displays properties that can disrupt cellular membranes and alter permeability. This mechanism is beneficial in enhancing the penetration of other therapeutic agents in topical formulations. However, its irritant potential on skin and mucous membranes should be noted, as it can lead to dryness and irritation with prolonged exposure.

Pharmacokinetics

Lauryl sulfate is primarily applied topically and is not intended for systemic absorption. When used in formulations, it acts locally at the site of application. Its absorption through the skin is minimal, and any systemic exposure is limited. Metabolism and excretion pathways are not well-defined for topical applications, as it is largely washed away after use.

Pregnancy

Safety during pregnancy has not been established. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Unknown whether lauryl is excreted in human 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.

Indications

• Used as a filler in tablet formulations
• Serves as a binder in solid dosage forms
• Acts as a disintegrant to aid tablet dissolution
• Improves flow properties of powders in manufacturing

Dosage

Children: Refer to specific formulations and guidelines for dosing, as microcrystalline cellulose is used as an excipient and does not have a standard dosing regimen.

Adults: Refer to specific formulations and guidelines for dosing, as microcrystalline cellulose is used as an excipient and does not have a standard dosing regimen.

Mechanism of action

Microcrystalline cellulose functions primarily as a bulking agent and a stabilizer in pharmaceutical formulations. It does not exert pharmacological effects on its own but serves to provide structure and stability to the drug formulations, facilitating the release of the active pharmaceutical ingredient (API) during dissolution and absorption.

Pharmacodynamics

MCC does not have a pharmacodynamic profile as it is not an active drug. Its role is to enhance the physical properties of pharmaceutical products, ensuring uniformity, consistency, and stability of the drug formulation. Its ability to absorb water and swell aids in the disintegration of tablets in the gastrointestinal tract, promoting the release of the active ingredients.

Pharmacokinetics

As a non-digestible polysaccharide, microcrystalline cellulose is not absorbed in the gastrointestinal tract. It passes through the digestive system unchanged and is excreted in the feces. Its presence in the gastrointestinal tract can have a bulking effect, promoting bowel regularity without contributing calories.

Pregnancy

Microcrystalline cellulose is generally considered safe for use during pregnancy as it is not absorbed and is used as an excipient.

Breast-feeding

Microcrystalline cellulose is also considered safe during breastfeeding since it is not absorbed into the systemic circulation.

Storage

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

Formulations

• Tablets
• Capsules
• Powder

Indications

• Constipation
• Dry skin
• Skin irritation

Dosage

Children: Refer to specific guidelines and prescribing information for paediatric dosing.

Adults: Refer to specific guidelines and prescribing information for adult dosing.

Mechanism of action

Paraffin acts as a lubricating agent in the gastrointestinal tract. It coats the stool and the intestinal walls, which helps to ease the passage of feces by reducing friction. This action promotes bowel movements and alleviates constipation. When used topically, it forms a barrier on the skin, which helps to retain moisture and protect against irritants.

Pharmacodynamics

Paraffin has a low viscosity and surface tension, which allows it to spread easily over surfaces. Its lubricating properties facilitate the movement of stool through the intestines, while its emollient properties help in maintaining skin hydration and barrier function. The onset of action for oral administration typically occurs within 6 to 8 hours, making it effective in treating occasional constipation.

Pharmacokinetics

Paraffin is not absorbed systemically when ingested; it remains in the gastrointestinal tract and is excreted unchanged in the feces. After oral administration, it acts locally in the intestines without significant systemic effects. When used topically, it remains on the skin surface and does not penetrate deeply, providing a protective layer without altering systemic pharmacokinetics.

Adverse effects

• Abdominal cramps
• Diarrhea
• Nausea
• Vomiting
• Lipid pneumonia (when aspirated)
• Electrolyte imbalances

Precautions

• Use with caution in patients with gastrointestinal obstruction
• Avoid in patients with a history of aspiration
• Monitor for signs of dehydration with prolonged use

Pregnancy

Use only if clearly needed. Consult a healthcare provider for advice.

Breast-feeding

Paraffin can be excreted in breast milk, use with caution.

Storage

Store at room temperature away from moisture and heat.

Formulations

• Liquid paraffin
• Soft paraffin (for topical use)

Indications

• Preoperative skin antisepsis
• Wound irrigation and cleansing
• Management of minor cuts and abrasions
• Treatment of minor skin infections
• Disinfection of mucous membranes

Dosage

Children: Refer to specific product guidelines for concentration and application method, as doses may vary by formulation.

Adults: Refer to specific product guidelines for concentration and application method, as doses may vary by formulation.

Mechanism of action

Povidone-iodine exerts its antiseptic effects primarily through the release of free iodine, which penetrates microbial cell walls and disrupts protein and nucleic acid synthesis. This leads to cell lysis and death of a wide variety of pathogens. The mechanism involves the oxidation of essential cellular components, thus rendering microorganisms inactive.

Pharmacodynamics

Povidone-iodine demonstrates rapid bactericidal activity, effectively reducing the microbial load on the skin and in wounds. The antimicrobial efficacy is influenced by factors such as concentration, exposure time, and the presence of organic matter. Its broad-spectrum action makes it effective against gram-positive and gram-negative bacteria, fungi, and viruses, making it a versatile antiseptic.

Pharmacokinetics

Povidone-iodine is not significantly absorbed through intact skin; however, some absorption may occur with large or prolonged applications, especially on compromised skin. The elimination half-life of iodide is approximately 24 hours, with the majority excreted unchanged in the urine. Iodine levels can be temporarily elevated in the serum after application, particularly in patients with pre-existing thyroid conditions.

Contra-indications

• Hypersensitivity to povidone-iodine or any of the excipients
• Thyroid dysfunction
• Use in infants less than 2 months of age

Adverse effects

• Skin irritation
• Burning sensation
• Allergic reactions
• Staining of skin and clothing
• Thyroid dysfunction
• Electrolyte imbalance (with prolonged use)

Interactions

• May interfere with thyroid function tests
• Incompatibility with other antiseptics or disinfectants

Precautions

• Avoid contact with eyes
• Use with caution in patients with thyroid disease
• Not for deep puncture wounds or serious burns

Pregnancy

Generally considered safe for topical use, but should be used with caution. Consult a healthcare professional for guidance.

Breast-feeding

Suitable for topical use, but excessive use should be avoided. Consult a healthcare professional for guidance.

Storage

Store at room temperature, away from direct sunlight. Keep container tightly closed.

Formulations

• Topical solution
• Ointment
• Surgical scrub
• Swab sticks

Indications

• Hyperthyroidism
• Graves' disease
• Thyroid storm

Dosage

Children: Refer to the BNF

Adults: The usual initial dose of propylthiouracil in adults is 300 mg per day, divided into 3 doses. The maintenance dose is typically 100-150 mg per day, adjusted based on thyroid function tests.

Mechanism of action

Propylthiouracil acts by inhibiting the enzyme thyroid peroxidase, which is involved in the iodination of tyrosine residues in thyroglobulin, a precursor of thyroid hormones. By blocking this enzyme, PTU reduces the production of thyroxine (T4) and triiodothyronine (T3), leading to decreased thyroid hormone levels in circulation. Additionally, PTU inhibits the conversion of T4 to T3 in peripheral tissues, further contributing to its antithyroid effects.

Pharmacodynamics

The pharmacodynamic effects of propylthiouracil are primarily centered around its ability to lower thyroid hormone levels, which helps alleviate symptoms of hyperthyroidism such as increased heart rate, weight loss, and anxiety. The onset of action can vary, but therapeutic effects may be observed within several weeks of initiation. Monitoring thyroid function tests is essential to assess the efficacy and adjust dosing as needed.

Pharmacokinetics

Propylthiouracil is well absorbed from the gastrointestinal tract, though its bioavailability can be affected by factors such as food intake. The drug is extensively metabolized in the liver, and its elimination half-life averages around 1-2 hours. Most of the drug is excreted in urine as metabolites. It is important to note that due to its rapid metabolism, multiple daily doses may be required to maintain therapeutic levels.

Interactions

• propylthiouracil+metyrapone: Severe (decreases effects)

Dosage

Children: Phthalates are not indicated for any medical use and thus do not have established dosing guidelines.

Adults: Phthalates are not indicated for any medical use and thus do not have established dosing guidelines.

Mechanism of action

Phthalates exert their effects primarily through the modulation of hormonal pathways. They are known to interfere with the endocrine system by mimicking or inhibiting the action of hormones, particularly sex hormones like testosterone. This can lead to developmental and reproductive toxicity, affecting both male and female reproductive systems.

Pharmacodynamics

Phthalates are lipophilic compounds that can be absorbed through the skin, ingested, or inhaled. Once in the body, they may bind to various nuclear receptors and influence gene expression related to hormone regulation. Their potential to disrupt endocrine function poses risks for various health outcomes, including reproductive and developmental issues.

Pharmacokinetics

Phthalates are rapidly absorbed and metabolized in the human body. They undergo hydrolysis to form mono-phthalates, which are the active metabolites responsible for their biological effects. These metabolites are then conjugated and excreted primarily in the urine. The half-life of phthalates can vary, but they are generally considered to have a short elimination half-life due to their rapid metabolism.

Pregnancy

Limited data on the safety of phthalates during pregnancy. Some studies suggest potential risks, but evidence is not conclusive.

Breast-feeding

Limited information available regarding the excretion of phthalates in human milk. Caution is advised when considering use during breastfeeding.

Storage

Store in a cool, dry place away from light. Specific storage conditions may vary based on formulation.

Indications

• Nutritional supplementation
• Energy source in enteral nutrition
• Excipient in pharmaceutical formulations

Dosage

Children: Refer to specific guidelines or product inserts for dosing information, as it can vary based on the context of use.

Adults: Refer to specific guidelines or product inserts for dosing information, as it can vary based on the context of use.

Mechanism of action

Starch is broken down into glucose units by enzymes such as amylase during digestion. The glucose is then absorbed in the intestines and utilized for energy production in the body's cells. This pathway involves hydrolysis of the glycosidic bonds, converting starch into simpler sugars.

Pharmacodynamics

Starch primarily serves as an energy source. Its digestion and absorption lead to an increase in blood glucose levels, which provides energy for metabolic processes. In this context, it plays a crucial role in maintaining energy homeostasis in the body.

Pharmacokinetics

Starch is not absorbed in its polymeric form; it must first be enzymatically hydrolyzed into simpler sugars such as maltose and glucose. The digestion and absorption of starch occur predominantly in the small intestine, with glucose being readily absorbed into the bloodstream. The rate of absorption can vary depending on the type of starch and its physical form.

Adverse effects

• Allergic reactions
• Gastrointestinal discomfort
• Diarrhea
• Constipation

Precautions

• Use with caution in individuals with known allergies to starch or starch derivatives
• Monitor for gastrointestinal symptoms in patients with a history of digestive disorders

Pregnancy

Starch is generally considered safe for use during pregnancy. However, it should be consumed in moderation as part of a balanced diet.

Breast-feeding

Starch is deemed safe for nursing mothers when used in moderation as part of a balanced diet.

Storage

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

Formulations

• Powder
• Granules
• Tablets
• Suspensions

Indications

• Orthopedic implants
• Dental implants
• Prosthetic devices
• Surgical instruments

Mechanism of action

Titanium does not have a specific mechanism of action as it is not a drug in the traditional sense. Instead, its biocompatibility allows it to integrate with biological tissues without eliciting significant immune responses, making it suitable for use in implants and prosthetic devices. The presence of titanium ions can influence biological processes, including cell proliferation and differentiation.

Pharmacodynamics

Titanium itself does not exhibit pharmacodynamics as it is not administered as a drug. Its interactions within biological systems are primarily mechanical and structural, providing support and stability in orthopedic and dental applications. The biocompatibility of titanium allows for favorable tissue integration and reduced rejection rates compared to other materials.

Pharmacokinetics

As titanium is not a pharmacological agent, traditional pharmacokinetic parameters such as absorption, distribution, metabolism, and excretion do not apply. Titanium is typically utilized in solid forms, such as implants, where it remains localized and does not undergo metabolism or systemic circulation.

Pregnancy

There is limited data on the use of titanium during pregnancy. Consult a healthcare professional before use.

Breast-feeding

There is limited data on the excretion of titanium in breast milk. Consult a healthcare professional before use.

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

Although the exact mechanism of action is unknown, praziquantel was hypothesized to target the β subunits of voltage-gated Ca₂₊ channels, particularly in Schistosoma mansoni and Schistosoma japonicum, due to the lack of two conserved serine residues in these subunits. This is supported by the finding that co-administration of calcium channel blockers like nicarpidine and nifedipine renders 50% of Schistosoma mansoni resistant to praziquantel. Increased exposure of antigens on the worm surface was also observed, but little research has been done to elucidate on the mechanism of action.

Pharmacodynamics

In vitro studies on trematodes and cestodes have shown that praziquantel induces a rapid contraction of schistosomas by a specific effect on the permeability of the cell membrane. The drug further causes vacuolization and disintegration of the schistosome tegument. The effect is more marked on adult worms compared to young worms. An increased Ca2⁺-influx may play an important role. Secondary effects are inhibition of glucose uptake, lowering of glycogen levels and stimulation of lactate release. The action of praziquantel is specific to trematodes and cestodes; nematodes (including filariae) are not affected. Praziquantel is active against schistosoma (for example, Schistosoma mekongi, Schistosoma japonicum, Schistosoma mansoni and Schistosoma hematobium), and infections due to the liver flukes, Clonorchis sinensis/Opisthorchis viverrini. Published in vitro data have shown a potential lack of efficacy of praziquantel against migrating schistosomulae. An interesting quirk of praziquantel is that it is relatively ineffective against juvenile schistosomes. While initially effective, effectiveness against schistosomes decreases until it reaches a minimum at 3-4 weeks. Effectiveness then increases again until it is once again fully effective at 6-7 weeks.

Mechanism of action

The feasibility of an oxygen-independent mechanism of chloroform bioactivation was indicated by the covalent binding to lipid and protein occurring in anaerobic incubations of chloroform and microsomes in the presence of NADPH. Under these conditions, the loss of cytochrome p450 and the inhibition of related mono-oxygenases were also observed. The chloroform anoxic biotransformation was negligible in uninduced microsomes and seemed to be catalyzed mainly by phenobarbital-inducible p450 isozymes. Biotransformation could also be supported by NADH as the source of reducing equivalents. Anaerobic metabolism of chloroform led to decreased levels of the main phenobarbital-induced p450 isozymes even at low chloroform concentration, and did not affect benzo(a)pyrene hydroxylase activity. These effects were not decreased by thiolic compounds. The oxidation products of chloroform caused a general impairment of the monoxygenase system, probably related to the formation of protein aggregates with very high molecular weight. In the presence of physiological concentrations of GSH, the targets of aerobically-produced metabolite were lipids, and, to a smaller extent, p450. At low chloroform concentrations and/or in the presence of GSH, the most changes to microsomal structures seemed to be produced by the reductively-formed intermediates.

Mechanism of action

The mechanism by which methylene chloride induces mammary adenomas in the rat is important for human hazard assessment. Female Sprague- Dawley rats receiving methylene chloride have a high blood level of prolactin. In common with the response to other agents which act via hyperprolactinaemia, the methylene chloride-induced response is of benign neoplasms only. There is no evidence for the binding of methylene chloride to the DNA of other tissues and hence it seems unlikely that it will bind to mammary tissue when the primary site of metabolism is the liver. It seems most likely, therefore, that the increased incidence of mammary adenomas is the result of an indirect mechanism operating via hyperprolactinaemia. Dichloromethane (DCM) is a hepatic and pulmonary carcinogen in mice exposed to high doses by inhalation. It has been shown previously that the incidence of liver and lung tumors does not increase in rats or hamsters exposed to the dihaloalkane under conditions similar to those that produced tumors in mice. The biological consequences of DCM exposure to humans is therefore uncertain. The carcinogenic effects of DCM in the mouse are caused by the interaction with DNA of a glutathione (GSH) conjugate that is produced by the class theta glutathione S-transferase T1-1 (GST T1-1). The species specificity is thought to be due to the greater amount of transferase activity in mouse target organs and specific nuclear localization of GST T1-1 in target cells. This paper directly compares the relative capacity and locality of DCM activation in mouse and human tissues. The results show that mouse GST T1-1 is more efficient in catalyzing the conjugation of DCM with GSH than the orthologous human enzyme. In addition, the mouse expresses higher levels of the transferase than humans in hepatic tissue. Histochemical analysis confirmed the presence of GST T1-1 in the nucleus of mouse liver cells. However, in human liver GST T1-1 was detected in bile duct epithelial cells and hepatocyte nuclei but was also present in the cytoplasm. Taking this information into account, it is unlikely that humans have a sufficiently high capacity to activate DCM for this compound to be considered to represent a carcinogenic risk. Dichloromethane (DCM) is considered a probable human carcinogen. Laboratory studies have shown an increased incidence of lung and liver cancer in mice but not in rats or hamsters. Despite the correlation between metabolism of DCM by the glutathione-S-transferase (GST) pathway and the occurrence of tumors in different species, the mechanism of tumor induction by DCM metabolites produced through the GST pathway remains unclear. In this study a V79 cell line stably transfected with the murine GST theta 1 gene (mGSTT1) was compared to the parent cell line (MZ) to determine how the construct affects DCM metabolism and the sensitivity of the cell line to DNA damage and cytotoxicity. V79 cells were treated with DCM (2.5-10mM) or formaldehyde (150-600muM) for 2hr. Also, formaldehyde produced by V79 cytosol metabolism of DCM was measured spectrophotometrically. DNA damage and DNA-protein crosslinks were measured by the standard and proteinase K-modified alkaline single cell gel electrophoresis (SCG) assays. Cytotoxicity was assessed by trypan blue stain exclusion, the Live/Dead((R)) cell viability/cytotoxicity kit for animal cells, and the neutral red assay. After DCM treatment a significant concentration-dependent increase in tail moment in the V79 MZ cells was observed compared to a significant concentration-dependent decrease in tail moment in the V79 mGSTT1 cells. Post-incubation with proteinase K significantly increased DNA migrations in DCM-treated V79 mGSTT1 cells. DCM formed significantly higher levels of formaldehyde in the cytosol of the V79 mGSTT1 cells than in the cytosol of the V79 MZ cells. Results using the cytotoxicity assays were comparable using the trypan blue and Live/Dead((R)) assays, neither showing a difference in resp

Mechanism of action

...Not infrequently intentional butane inhalation results in high morbidity and mortality. A fatal outcome of butane abuse can be caused by asphyxia, cardiac arrhythmia or trauma. The reported number of cases in which death was the consequence of pure butane inhalation is limited, and in most cases a mixture of propellants was involved. This report covers two cases of sudden death due to the sniffing of a cigarette lighter refill containing butane. Autopsy was followed by toxicological, pathohistological and immunohistochemical analysis. Butane gas was confirmed in samples of blood, urine, brain and lungs... Histology showed almost identical changes in the lungs and heart in both cases. The morphology of heart damage on standard H/E stains was of special interest because it displayed all the characteristics of chronic and acute myocardial hypoxia found in the absence of atherosclerotic heart disease. In order to confirm early cardiac death caused by asphyxia due to butane inhalation a panel of immunohistochemical agents was used...

Mechanism of action

Ethylene glycol toxicity results from its metabolism to glycolic acid and other toxic metabolites. The accumulation of glycolate and the elimination kinetics of ethylene glycol and its metabolites are not well understood, so studies with male Sprague-Dawley rats and mixed breed dogs have been carried out. Ethylene glycol was administered by gavage to rats and dogs which were placed in metabolic cages for urine and blood sample collection at timed intervals. The peak plasma level of ethylene glycol occurred at 2 hr after dosing and that of glycolate between 4-6 hr. The rate of ethylene glycol elimination was somewhat faster in rats with a half-life of 1.7 hr compared to 3.4 hr in dogs. The maximum plasma level of glycolate was greater in rats although the pattern of accumulation was similar to that in dogs. Glycolate disappeared from the plasma at the same time as ethylene glycol, suggesting a slower rate of elimination of the metabolite than that of ethylene glycol. Renal excretion of ethylene glycol was an important route for its elimination accounting for 20-30% of the dose. Renal excretion of glycolate represented about 5% of the dose. Ethylene glycol induced an immediate, but short lived diuresis compared to that in control rats. Minimal clinical effects (mild acidosis with no sedation) were noted at these doses of ethylene glycol (1-2 g/kg) in both rats and dogs. The results indicate that the toxicokinetics of ethylene glycol and glycolate were similar in both species. The effect of 0.35 to 0.8 mmol/kg glycolic acid and 1.0 to 4.4 mmol/kg sodium glycolate on cyclopropane-epinephrine induced cardiac arrhythmias was examined using dogs. Doses of 0.35 to 0.5 mmol/kg glycolic acid increased the duration of arrhythmias in the 13 dogs tested, whereas doses >0.5 mmol/kg decreased or totally eliminated the arrhythmias in each of 11 dogs. Depression was observed for many of the dogs at higher doses. Sodium glycolate was much less effective in decreasing the arrhythmias, with 3 mmol/kg being required and its action being transient.