TESS

Indications

• Eczema
• Psoriasis
• Contact dermatitis
• Allergic dermatitis
• Seborrheic dermatitis

Dosage

Children: Refer to specific product information or clinical guidelines for appropriate dosing in children, as it varies by formulation and condition treated.

Adults: Refer to specific product information or clinical guidelines for appropriate dosing, as it varies by formulation and condition treated.

Mechanism of action

Acetonide exerts its effects by binding to glucocorticoid receptors in the cytoplasm of target cells, leading to the translocation of the receptor-ligand complex into the nucleus. This complex then influences the expression of specific genes, resulting in decreased production of pro-inflammatory cytokines and increased production of anti-inflammatory proteins. This modulation of gene expression contributes to its anti-inflammatory and immunosuppressive effects.

Pharmacodynamics

The pharmacodynamics of acetonide involve its ability to inhibit the migration of leukocytes to sites of inflammation, reduce the production of inflammatory mediators such as prostaglandins and leukotrienes, and suppress the immune response. The potency and duration of action can vary based on the specific formulation and concentration used.

Pharmacokinetics

Acetonide is absorbed through the skin when applied topically, with systemic absorption depending on the formulation, application area, and duration of use. It undergoes hepatic metabolism, and its metabolites are excreted primarily through the urine. The half-life and clearance rates can vary based on individual patient factors and specific formulations.

Contra-indications

• Hypersensitivity to acetonide or any component of the formulation.
• Active or untreated infections at the site of application.

Adverse effects

• Local irritation or burning sensation at the application site.
• Skin thinning or atrophy with prolonged use.
• Systemic effects such as adrenal suppression with high doses or prolonged therapy.

Interactions

• Increased risk of systemic effects when used with other corticosteroids.
• Potentially altered metabolism when administered with CYP3A4 inhibitors or inducers.

Precautions

• Use with caution in patients with a history of tuberculosis or other infections.
• Monitor for signs of adrenal insufficiency in patients on high doses.
• Avoid application to large areas of the body or under occlusive dressings.

Pregnancy

Acetonide should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Consult with a healthcare professional before use.

Breast-feeding

Limited data available. Use with caution as it may be excreted in breast milk. Consult with a healthcare professional before use.

Storage

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

Formulations

• Topical cream
• Topical ointment
• Topical solution

Indications

• Dyspepsia
• Flatulence
• Bloating
• Cough relief
• Antimicrobial support

Dosage

Children: Consult appropriate pediatric herbal guidelines, as specific dosing is not universally established.

Adults: Refer to herbal supplement guidelines for dosing, as specific doses can vary widely based on preparation and concentration.

Mechanism of action

Aniseed contains several active compounds, including anethole, which is believed to exert its effects primarily through modulation of the gastrointestinal system. Anethole can stimulate the secretion of digestive enzymes and has been shown to possess antispasmodic properties, potentially alleviating symptoms related to gastrointestinal discomfort. Additionally, its antimicrobial properties may contribute to inhibiting the growth of certain pathogens.

Pharmacodynamics

The pharmacodynamic profile of aniseed is characterized by its ability to enhance digestive function and alleviate symptoms of dyspepsia. Its antispasmodic effects are mediated through inhibition of smooth muscle contractions in the gut. Aniseed may also exhibit mild sedative properties, contributing to its use as a calming herbal remedy. The overall effect is a combination of digestive support and potential relief from gastrointestinal discomfort.

Pharmacokinetics

The pharmacokinetics of aniseed components, particularly anethole, involve oral absorption followed by distribution throughout the body. Anethole is metabolized in the liver and excreted primarily in the urine. The onset of action can vary based on the form of administration, with herbal teas generally producing effects within a few hours, while concentrated extracts may have a more rapid onset. The duration of action is also influenced by the dose and form used.

Adverse effects

• Allergic reactions
• Dermatitis
• Gastrointestinal upset

Interactions

• May interact with anticoagulants, increasing the risk of bleeding
• Can enhance the effects of sedative medications

Precautions

• Use with caution in individuals with a history of allergies, particularly to plants in the Apiaceae family
• May cause skin irritation in sensitive individuals

Pregnancy

Generally considered safe when used in culinary amounts, but high doses should be avoided due to potential hormonal effects.

Breast-feeding

Considered safe when used in culinary amounts, but high doses should be avoided.

Storage

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

Formulations

• Whole seeds
• Essential oil
• Ground powder

Dosage

Children: Refer to specific formulations and usages, as dosing can vary widely depending on the application and regulatory guidelines.

Adults: Refer to specific formulations and usages, as dosing can vary widely depending on the application and regulatory guidelines.

Mechanism of action

Butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) act as antioxidants by inhibiting the oxidation of lipids. They scavenge free radicals and donate hydrogen atoms to reactive species, thus stabilizing and preventing oxidative damage to cellular components. This action helps to protect the integrity of cell membranes and prevent the formation of harmful peroxides.

Pharmacodynamics

The pharmacodynamic properties of butylated compounds are primarily related to their antioxidant activity. They exhibit a dose-dependent ability to inhibit lipid peroxidation, which is crucial in protecting cells from oxidative stress. Furthermore, they may modulate certain biochemical pathways involved in cell signaling and apoptosis, although these effects are less well-characterized.

Pharmacokinetics

Butylated compounds are absorbed from the gastrointestinal tract following oral ingestion. They undergo metabolic processing primarily in the liver, where they are conjugated and excreted in urine. The half-life of butylated compounds in humans is variable, influenced by factors such as dosage and individual metabolism. Accumulation in tissues is generally low, but prolonged exposure may lead to higher tissue concentrations.

Adverse effects

• Gastrointestinal disturbances
• Allergic reactions
• Potential carcinogenic effects with prolonged exposure

Precautions

• Use with caution in patients with a history of hypersensitivity to butylated compounds
• Avoid prolonged exposure due to potential toxicity

Pregnancy

Limited data available, use only if the benefits outweigh the risks.

Breast-feeding

Unknown, exercise caution and consult a healthcare provider.

Storage

Store in a cool, dry place away from light.

Formulations

• Butylated hydroxytoluene (BHT)
• Butylated hydroxyanisole (BHA)

Indications

• Topical formulations for skin conditions
• Ophthalmic preparations
• Oral drug delivery systems
• Cosmetic products

Dosage

Children: Refer to specific product guidelines for dosing recommendations, as dosage can vary based on formulation and intended use.

Adults: Refer to specific product guidelines for dosing recommendations, as dosage can vary based on formulation and intended use.

Mechanism of action

Carbopol acts by forming a gel-like consistency when mixed with water, which allows for the sustained release of active ingredients. The polymer structures create a network that traps water, leading to increased viscosity. This property can enhance the stability and efficacy of various formulations, including topical and oral medications.

Pharmacodynamics

Carbopol is non-toxic and biocompatible. It does not exhibit pharmacological activity on its own but influences the pharmacokinetics of other drugs by modifying the release rate and absorption characteristics. Its gel-forming ability can improve the adhesion of topical agents to the skin, enhancing local therapeutic effects.

Pharmacokinetics

Carbopol is not absorbed systemically when applied topically, as it remains localized at the application site. Its viscosity and gel-forming properties affect the diffusion of drugs from the formulation, which can alter the rate of drug release and absorption. When used in oral formulations, it can modify the dissolution profile of the active ingredients.

Pregnancy

Carbopol is generally considered safe during pregnancy, but it is advisable to consult a healthcare provider before use.

Breast-feeding

Carbopol is not absorbed systemically, thus it is unlikely to pose any risk during breastfeeding, but consulting a healthcare provider is recommended.

Storage

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

Formulations

• Carbopol 940
• Carbopol 941
• Carbopol 980

Indications

• Constipation
• Labor induction
• Topical treatment for skin conditions

Dosage

Children: Refer to the BNF for Children for appropriate pediatric dosing guidelines, as no specific doses are provided.

Adults: Refer to specific guidelines for adult dosing based on the formulation used and the condition being treated, as no standardized dose is provided.

Mechanism of action

Ricinoleic acid, the main active component of castor oil, acts as a stimulant laxative. It works by increasing the peristaltic movement of the intestines, which aids in the evacuation of stool. Additionally, it may inhibit the absorption of water in the intestines, resulting in softer stools. The oil is also believed to have anti-inflammatory properties, which can be beneficial in treating certain skin conditions.

Pharmacodynamics

The pharmacodynamic properties of castor oil include its ability to stimulate intestinal motility and increase the secretion of intestinal fluids. This leads to a faster transit time for stool through the bowel. In topical applications, castor oil exhibits emollient and moisturizing effects, promoting healing and soothing irritated skin. Its anti-inflammatory effects may also contribute to the reduction of swelling and pain in inflamed tissues.

Pharmacokinetics

Castor oil is absorbed in the gastrointestinal tract, where it is metabolized to ricinoleic acid. The onset of action for its laxative effect typically occurs within 2 to 6 hours after oral administration. The duration of action varies, but effects usually last for several hours. When applied topically, castor oil penetrates the skin and may provide localized effects without significant systemic absorption.

Adverse effects

• Abdominal cramps
• Diarrhea
• Nausea
• Vomiting
• Dehydration

Precautions

• Use with caution in patients with gastrointestinal disorders
• Not recommended for prolonged use
• Monitor for signs of dehydration

Pregnancy

Castor oil is generally not recommended during pregnancy due to potential uterine contractions and risk of premature labor.

Breast-feeding

Castor oil should be used with caution during breastfeeding as it may cause gastrointestinal discomfort in nursing infants.

Storage

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

Formulations

• Liquid
• Capsules

Indications

• Acidulant in food and beverages
• Preservative in pharmaceutical formulations
• pH adjuster in various chemical preparations

Dosage

Children: Refer to product-specific guidelines for appropriate dosing based on formulation and indication.

Adults: Refer to product-specific guidelines for appropriate dosing based on formulation and indication.

Mechanism of action

Citric acid acts by chelating metal ions, which can enhance the solubility of certain compounds and improve their bioavailability. It also contributes to the acidity of the environment, which can influence enzymatic activity and metabolic pathways, particularly in the degradation of citronellol.

Pharmacodynamics

Citric acid exhibits mild pharmacological effects primarily attributed to its role in metabolic processes. It aids in the regulation of pH levels, which can impact enzymatic reactions and biochemical pathways. The acid's chelating properties may help to reduce the toxicity of certain metal ions in biological systems.

Pharmacokinetics

Citric acid is rapidly absorbed after oral administration and is metabolized in the liver. It undergoes conversion to various metabolites in the citric acid cycle, contributing to energy production. The elimination primarily occurs through urine, with minimal accumulation in the body.

Pregnancy

Citric acid is generally regarded as safe during pregnancy when used in food amounts. However, consult a healthcare provider for advice on medicinal use.

Breast-feeding

Citric acid is considered safe during breastfeeding when consumed in food amounts. For medicinal use, consult a healthcare provider.

Storage

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

Indications

• Electrolyte replacement
• Volume expansion in hypovolemic patients
• Management of hyponatremia
• Support in intravenous fluid therapy

Dosage

Children: Refer to the BNF for Children for appropriate dosing in paediatric patients, as dosages may vary based on the formulation and clinical condition.

Adults: Refer to specific product information or clinical guidelines for dosage recommendations, as disodium is often part of combination products.

Mechanism of action

Disodium compounds often function by providing sodium ions that are essential for various physiological processes. Sodium ions play a critical role in maintaining osmotic balance, nerve impulse transmission, and muscle contraction. In the context of intravenous solutions, disodium helps to restore electrolyte balance in patients.

Pharmacodynamics

The pharmacodynamics of disodium is primarily related to its role in electrolyte balance and fluid homeostasis. Sodium ions are vital for the function of excitable tissues, including neurons and muscle cells. Changes in sodium levels can affect blood pressure, hydration status, and overall cellular function.

Pharmacokinetics

The pharmacokinetics of disodium compounds depend on their specific formulation and route of administration. When administered intravenously, disodium is rapidly distributed in the extracellular fluid, where it helps to maintain osmotic pressure. Sodium is primarily excreted by the kidneys, and its levels can be influenced by fluid intake, dietary sodium, and renal function.

Pregnancy

Use with caution. Consult a healthcare provider for specific guidance.

Breast-feeding

Use with caution. Consult a healthcare provider for specific guidance.

Storage

Store at room temperature, away from moisture and direct sunlight.

Indications

• Lead poisoning
• Mercury poisoning
• Calcium overload
• Certain diagnostic procedures involving heavy metals

Dosage

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

Adults: Refer to the BNF for specific dosing guidelines based on the condition being treated, considering factors such as the severity of metal poisoning and renal function.

Mechanism of action

Edetate functions by forming stable complexes with divalent and trivalent metal ions, including lead and calcium, through its multiple carboxylate and amine groups. This chelation renders the metals more soluble and promotes their renal excretion, thereby reducing their toxic effects in the body.

Pharmacodynamics

The chelation of metals by edetate decreases the free metal concentration in the bloodstream, which mitigates the toxic effects associated with heavy metal accumulation. The efficacy of edetate in removing metals such as lead has been well documented, and its ability to bind calcium can influence calcium homeostasis in certain clinical scenarios.

Pharmacokinetics

Edetate is administered intravenously, with rapid distribution throughout the extracellular fluid. It is primarily excreted unchanged by the kidneys. The onset of action occurs quickly after administration, and the duration depends on the dose and the patient's renal function. The elimination half-life is approximately 1 hour but may vary based on renal clearance.

Contra-indications

• Hypersensitivity to edetate or any component of the formulation
• Severe renal impairment
• Active bleeding disorders

Adverse effects

• Hypocalcemia
• Nausea
• Vomiting
• Diarrhea
• Abdominal pain
• Headache
• Rash
• Fever

Interactions

• May enhance the effects of anticoagulants
• Concurrent use with calcium supplements may reduce effectiveness
• May interfere with the absorption of certain medications due to changes in gastrointestinal motility

Precautions

• Use with caution in patients with renal impairment
• Monitor electrolyte levels, particularly calcium, during treatment
• Assess the patient's hydration status before administration

Pregnancy

Limited data on the use of edetate in pregnancy. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Caution is advised as it is not known whether edetate is excreted in human milk. Weigh the risks and benefits before use.

Storage

Store in a cool, dry place, protected from light. Do not freeze.

Formulations

• Edetate disodium injection
• Edetate calcium disodium injection

Indications

• Enhancement of taste in food and beverages
• Improvement of palatability in nutritional products
• Masking undesirable flavors in medications

Dosage

Children: There is no specific pediatric dosage for flavor agents as they are used as needed to improve the taste of food and beverages.

Adults: There is no specific dosage for flavor agents as they are used as needed to achieve the desired taste and aroma in food and beverages.

Mechanism of action

Flavor compounds interact with taste receptors on the tongue, stimulating the sensory neurons responsible for taste perception. This interaction influences the overall flavor profile of food and beverages, enhancing the eating experience. Some flavors may also have a psychological effect, stimulating appetite or evoking pleasant memories associated with certain tastes.

Pharmacodynamics

While flavor agents are primarily used for sensory enhancement in food, their pharmacodynamic effects are minimal as they are not designed to elicit a pharmacological response. However, certain flavors may influence digestion and metabolism indirectly by enhancing saliva production or affecting gut motility. The enjoyment of flavored products can also lead to increased food intake and satisfaction.

Pharmacokinetics

Flavour compounds are typically ingested and metabolized by the body. Their absorption rates can vary depending on their chemical structure and formulation. Once ingested, they may be rapidly metabolized in the liver and other tissues, with excretion primarily via urine. The specific pharmacokinetic profiles of flavor agents can vary significantly based on their source and chemical properties.

Pregnancy

Flavours are generally considered safe for use during pregnancy, but specific assessments should be made based on the type of flavouring agent.

Breast-feeding

Most flavouring agents are deemed safe during breastfeeding, although it's advisable to consult healthcare professionals regarding specific ingredients.

Storage

Store in a cool, dry place away from direct sunlight and heat sources. Ensure that the container is tightly sealed to prevent contamination.

Dosage

Children: Refer to the BNF for Children for appropriate dosing information in paediatric cases, especially in instances of overdose.

Adults: Refer to the BNF for specific dosing information based on clinical circumstances, particularly in cases of overdose.

Mechanism of action

Ethylene glycol is metabolized by alcohol dehydrogenase to glycoaldehyde, which is subsequently converted to glycolic, glyoxylic, and oxalic acids. These metabolites contribute to anion gap metabolic acidosis and are responsible for tissue injury through the formation of insoluble calcium oxalate crystals.

Pharmacodynamics

The toxicity of ethylene glycol arises from its metabolites, particularly glycolic and oxalic acids. These compounds induce metabolic acidosis, lead to renal failure through calcium oxalate crystal deposition in the kidneys, and can cause neurological impairment. The anion gap increases due to the accumulation of these acids, leading to complications such as cardiovascular instability and potential multi-organ failure.

Pharmacokinetics

Ethylene glycol is rapidly absorbed after oral ingestion. It undergoes first-pass metabolism primarily in the liver, where it is converted into its toxic metabolites. The elimination half-life of ethylene glycol varies but is generally prolonged in cases of renal impairment. Renal excretion of metabolites contributes to the duration of toxicity, necessitating prompt medical intervention in cases of overdose.

Adverse effects

• Metabolic acidosis
• Renal failure
• CNS depression
• Hypocalcemia
• Cardiovascular collapse
• Pulmonary edema

Precautions

• Use with caution in patients with renal impairment
• Monitor for signs of metabolic acidosis
• Evaluate electrolyte levels, particularly calcium

Pregnancy

There is limited data on the safety of ethylene glycol in pregnancy. It should only be used if clearly needed.

Breast-feeding

It is unknown if ethylene glycol is excreted in human milk. Caution is advised.

Storage

Store in a tightly closed container at room temperature, away from heat and moisture.

Formulations

• Liquid

Dosage

Children: Paediatric dosing information is not standardized and should be derived from specific product guidelines or expert consultation.

Adults: Dosage and usage depend on the specific hydrogenated compound and its intended therapeutic application. Refer to specific product guidelines for detailed dosing information.

Mechanism of action

Hydrogenation alters the molecular structure of fatty acids, transforming double bonds into single bonds. This process increases the saturation level of fats, which can influence their metabolic pathways and lipid profiles in the body.

Pharmacodynamics

The pharmacodynamic effects of hydrogenated compounds depend on the specific substance being hydrogenated. Generally, hydrogenated fats can affect lipid metabolism, potentially leading to increased levels of LDL cholesterol and decreased levels of HDL cholesterol when consumed in excess. The physiological effects may include changes in insulin sensitivity and inflammatory responses.

Pharmacokinetics

The pharmacokinetics of hydrogenated compounds vary widely based on the specific hydrogenated product. Generally, these compounds are absorbed in the gastrointestinal tract, where they may undergo further metabolism by enzymes. The bioavailability, distribution, metabolism, and excretion depend on the fatty acid composition and the presence of other dietary components.

Pregnancy

Hydrogenated compounds, depending on their specific type, may have varying safety profiles in pregnancy. It is essential to consult specific guidelines or studies related to the particular hydrogenated substance in question.

Breast-feeding

The safety of hydrogenated compounds during breastfeeding may vary. Consultation with healthcare professionals regarding specific substances is advisable.

Storage

Hydrogenated substances should be stored in a cool, dry place, away from direct sunlight and heat to maintain stability.

Dosage

Children: Refer to specific guidelines for pediatric dosing; consult the BNF for Children for accurate dosage information.

Adults: Refer to specific guidelines for use; dosage may vary based on the context of use.

Mechanism of action

Hydroxide ions act primarily as bases, neutralizing acids to form water and salts. They participate in various biochemical pathways, including selenium metabolism and the degradation of reactive oxygen species. Hydroxide can influence enzyme activity and stability by altering the pH of the environment, thereby affecting metabolic reactions.

Pharmacodynamics

Hydroxide ions can impact biological processes by changing the local pH, which influences enzyme activity, ion transport, and the solubility of other compounds. Their ability to neutralize acids can help regulate physiological pH, contributing to homeostasis in living organisms.

Pharmacokinetics

As an inorganic ion, hydroxide does not undergo traditional pharmacokinetic processes like absorption, distribution, metabolism, or excretion. Instead, it is rapidly equilibrated in biological fluids and participates in acid-base reactions, having immediate effects on the local environment.

Pregnancy

There is limited information regarding the use of hydroxide during pregnancy. Consult a healthcare professional for advice.

Breast-feeding

Limited data is available on the excretion of hydroxide in breast milk. Consult a healthcare professional before use.

Storage

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

Indications

• Anxiety disorders
• Nausea and vomiting
• Allergic conditions
• Preoperative sedation
• Pruritus

Dosage

Children: Refer to the BNF for Children for appropriate dosing recommendations based on age and weight.

Adults: Refer to the BNF for specific dosing guidelines based on the indication and patient characteristics.

Mechanism of action

Hydroxyzine works by antagonizing the H1 histamine receptors, leading to a reduction in the effects of histamine in the body. This action helps alleviate symptoms of allergic reactions and promotes sedation. Additionally, it may exert effects on serotonin and adrenergic receptors, which could contribute to its anxiolytic properties. Hydroxyzine is also involved in various metabolic pathways, including selenium metabolism and the degradation of reactive oxygen species.

Pharmacodynamics

The pharmacodynamic effects of hydroxyzine include sedation, anxiolysis, and reduction of allergic symptoms. Its sedative effects can make it useful in managing anxiety and inducing sleep, while its antihistaminic properties help to relieve symptoms such as itching and rashes associated with allergic reactions. The onset of action is typically within 15 to 30 minutes when taken orally, with peak effects occurring within 1 to 2 hours.

Pharmacokinetics

Hydroxyzine is well absorbed from the gastrointestinal tract, with peak plasma concentrations occurring approximately 2 hours after oral administration. It is extensively metabolized in the liver, with metabolites, including cetirizine, possessing their own therapeutic effects. Hydroxyzine has a half-life of approximately 20 hours, allowing for once or twice daily dosing. It is primarily excreted in the urine, with less than 1% of the unchanged drug found in urine.

Interactions

• hydroxyzine+antiepileptics: Severe (increases risk of overheating and dehydration)
• hydroxyzine+zonisamide: Severe (increases risk of overheating and dehydration)
• hydroxychloroquine+penicillamine: Severe (increases risk of haematological toxicity)
• hydroxychloroquine+agalsidase alfa: Unknown (decreases effects)
• hydroxychloroquine+agalsidase beta: Unknown (decreases exposure)
• hydroxychloroquine+oral cholera vaccine: Unknown (decreases efficacy)
• live vaccines+hydroxy carbamide: Unknown (increases risk of generalised infection (possibly life-threatening))
• lanthanum+hydroxychloroquine: Unknown (decreases absorption)
• macrolides+hydroxychloroquine: Unknown (increases risk of serious cardiovascular adverse effects)
• hydroxychloroquine+remdesivir: Unknown (decreases effects)

Pregnancy

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

Breast-feeding

Use with caution. Hydroxychloroquine is excreted in breast milk, and effects on the infant are unknown.

Storage

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

Formulations

• Tablets
• Oral solution

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.

Indications

• Insecticide for agricultural use
• Research tool in toxicology

Dosage

Children: Refer to the BNF for Children for specific dosing and administration guidelines.

Adults: Refer to the BNF for specific dosing and administration guidelines.

Mechanism of action

Methyl parathion acts primarily by inhibiting the enzyme acetylcholinesterase, which is essential for the breakdown of the neurotransmitter acetylcholine. Its active metabolite, methyl paraoxon, is a potent inhibitor of both acetylcholinesterase and butyrylcholinesterase. The inhibition of these enzymes results in the accumulation of acetylcholine at synapses, leading to overstimulation of cholinergic receptors and resultant toxic effects.

Pharmacodynamics

The pharmacodynamics of methyl parathion involve its action as a noncompetitive inhibitor of acetylcholinesterase, causing prolonged effects of acetylcholine due to its inability to be hydrolyzed. The resultant cholinergic toxicity can lead to symptoms such as muscle twitching, respiratory distress, and potentially fatal outcomes if not treated promptly. The extent of inhibition is dose-dependent, with significant toxicity occurring after substantial enzyme inhibition.

Pharmacokinetics

Methyl parathion is absorbed through the gastrointestinal tract and can also be absorbed through the skin and respiratory tract. It is metabolized in the liver to form methyl paraoxon, which is responsible for the majority of its toxic effects. The distribution of methyl parathion in body tissues is influenced by its lipophilicity, and it is primarily excreted as metabolites in the urine. The elimination half-life and specific pharmacokinetic parameters can vary based on individual metabolism and exposure levels.

Pregnancy

There are no adequate and well-controlled studies in pregnant women. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether this drug is excreted in human milk. Caution is advised when administering to nursing women.

Storage

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

Formulations

• Liquid formulation

Indications

• Allergic conditions
• Autoimmune diseases
• Asthma and chronic obstructive pulmonary disease (COPD)
• Certain cancers (e.g., leukemia, lymphoma)
• Skin conditions (e.g., dermatitis)
• Inflammatory bowel disease
• Multiple sclerosis exacerbations
• Severe infections requiring immunosuppression

Dosage

Children: Refer to BNF for Children for specific dosing; doses vary significantly based on the child's age, weight, and condition being treated.

Adults: Refer to BNF for specific dosing; typically, initial doses range from 4 to 48 mg depending on the severity of the condition.

Mechanism of action

Methylprednisolone exerts its effects by binding to glucocorticoid receptors, leading to the modulation of gene expression. This interaction influences the transcription of anti-inflammatory proteins while suppressing the expression of pro-inflammatory genes, ultimately resulting in reduced inflammation and immune response.

Pharmacodynamics

The pharmacodynamic effects of methylprednisolone are characterized by its ability to decrease inflammation, suppress the immune response, and affect carbohydrate metabolism. Therapeutic doses lead to various systemic effects, including modification of leukocyte distribution and inhibition of cytokine production.

Pharmacokinetics

Methylprednisolone is well absorbed after oral administration, with a bioavailability of approximately 50%. It has a volume of distribution that reflects extensive tissue binding. The drug is metabolized primarily in the liver through conjugation and reduction, and its metabolites are excreted in urine. The half-life varies based on the route of administration but is generally around 18 to 36 hours.

Adverse effects

• Increased blood pressure
• Hyperglycemia
• Weight gain
• Mood changes
• Insomnia
• Gastrointestinal disturbances
• Increased susceptibility to infections

Interactions

• methylphenidate+apraclonidine: Severe (decreases effects)
• methylthioninium chloride+bupropion: Severe (increases risk of severe hypertension)
• methylphenidate+linezolid: Severe (increases risk of elevated blood pressure)
• rasagiline+methylphenidate: Severe (increases risk of a hypertensive crisis)
• mao-inhibitors+methylphenidate: Severe (increases risk of a hypertensive crisis)
• dronedarone+methylprednisolone: Moderate (increases exposure)
• miconazole+methylprednisolone: Moderate (increases concentration)
• antifungals, azoles+methylprednisolone: Moderate (increases exposure)
• crizotinib+methylprednisolone: Moderate (increases exposure)

Precautions

• Use with caution in patients with hypertension
• Monitor blood glucose levels in diabetic patients
• Consider potential for infection risk due to immunosuppression
• Evaluate for psychiatric effects in susceptible individuals

Pregnancy

Corticosteroids may be used during pregnancy if the potential benefit justifies the risk to the fetus. Careful monitoring is advised.

Breast-feeding

Corticosteroids are excreted in breast milk; caution is advised. Monitor the infant for potential effects.

Storage

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

Formulations

• Tablets
• Injectable solutions
• Topical preparations

Mechanism of action

Methylsulphate functions as a methylating agent, transferring a methyl group to nucleophiles. This process involves the formation of a sulfonium ion, which is highly reactive and can readily react with nucleophilic sites on various substrates, leading to methylation reactions.

Pharmacodynamics

The pharmacodynamics of methylsulphate is primarily related to its role as a methylating agent in biochemical reactions. It can alter the structure and function of biological molecules, potentially affecting cellular processes and signaling pathways. However, detailed pharmacodynamic studies specific to therapeutic use are limited.

Pharmacokinetics

There is limited information on the pharmacokinetics of methylsulphate, given its typical use as a reagent in laboratory settings rather than a clinical drug. When used in chemical reactions, its reactivity and transformation into other compounds would dictate its pharmacokinetic profile, which could vary significantly based on the specific context of use.

Pregnancy

There is limited data on the use of methylsulphate in pregnancy. Consult relevant guidelines.

Breast-feeding

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

Storage

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

Indications

• Preservative in cosmetics
• Preservative in pharmaceuticals
• Preservative in food products

Dosage

Children: Refer to specific product guidelines as dosing varies based on formulation and concentration used.

Adults: Refer to specific product guidelines as dosing varies based on formulation and concentration used.

Mechanism of action

Parabens work by inhibiting the growth of microorganisms through their ability to disrupt the cellular processes of bacteria and fungi. They penetrate the microbial cell membrane and disrupt enzyme and protein functions, leading to cell death. Parabens are known to have low toxicity and are metabolized by the body, subsequently being excreted in urine.

Pharmacodynamics

Parabens demonstrate broad-spectrum antimicrobial activity, making them effective preservatives in various formulations. Their efficacy is influenced by factors such as concentration, pH, and the presence of other ingredients in the formulation. Due to their structural similarity to estrogen, there has been concern regarding their potential endocrine-disrupting effects, although the clinical significance of this is still debated.

Pharmacokinetics

Parabens are readily absorbed through the skin and gastrointestinal tract. Once absorbed, they are rapidly metabolized primarily in the liver. They undergo hydrolysis to form para-hydroxybenzoic acid, which is then conjugated with glucuronic acid and excreted in urine. The half-life of parabens in the human body is relatively short, and they are eliminated rapidly.

Adverse effects

• Allergic reactions, such as skin rashes
• Irritation at the site of application
• Endocrine disruption (in high concentrations)

Precautions

• Use with caution in individuals with known sensitivities or allergies to parabens
• Consider potential endocrine effects with prolonged exposure

Pregnancy

Parabens are generally considered safe in cosmetics and personal care products during pregnancy, although caution is advised due to potential endocrine disruption.

Breast-feeding

Parabens are considered safe in breastfeeding, but it is recommended to use products with minimal or no parabens when possible.

Storage

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

Formulations

• Topical creams
• Lotions
• Shampoos
• Conditioners
• Makeup products
• Pharmaceutical preparations

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

• Constipation
• Bowel preparation before colonoscopy or surgery

Dosage

Children: Refer to specific product guidelines for dosing instructions.

Adults: Refer to specific product guidelines for dosing instructions.

Mechanism of action

Polyoxyl works by retaining water in the stool, increasing its bulk and consistency. This osmotic effect stimulates bowel movements by softening the stool and promoting peristalsis. The water-retaining properties are attributed to its high molecular weight and hydrophilicity, which allow it to attract and hold water within the gastrointestinal tract.

Pharmacodynamics

The pharmacodynamic profile of polyoxyl includes its ability to enhance stool water content, thereby improving fecal passage through the intestines. This results in increased stool frequency and decreased transit time. Polyoxyl does not significantly affect electrolyte balance, making it a safe option for chronic constipation management.

Pharmacokinetics

Polyoxyl is not absorbed systemically; it remains in the gastrointestinal tract where it exerts its effects. The onset of action can vary but typically occurs within 24 to 72 hours after administration. The elimination of polyoxyl occurs through fecal excretion, with no significant metabolism or renal clearance involved.

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Abdominal cramps
• Allergic reactions

Precautions

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

Pregnancy

Polyoxyl is generally regarded as safe for use during pregnancy, but specific clinical guidance should be consulted.

Breast-feeding

Polyoxyl is considered safe during breastfeeding, though maternal factors should be assessed.

Storage

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

Formulations

• Oral solution
• Tablet
• Topical cream

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)

Indications

• Plant growth regulation
• Agricultural applications as a growth inhibitor

Dosage

Children: Not applicable.

Adults: Refer to the relevant agricultural guidelines for specific applications.

Mechanism of action

In an in vitro study, propylene acts as a plant growth inhibitor by inhibiting the oxidation of indole-3-acetic acid by peroxidase in the presence of superoxide anion radicals. This inhibition is linked to the activation of an iron complex (compound III) shuttle, which enhances the reaction rate between superoxide and peroxidase, ultimately affecting plant growth processes. Propylene is a less effective inhibitor compared to ethylene.

Pharmacodynamics

The pharmacodynamic effects of propylene are primarily observed in its role as a growth inhibitor in plants. By modulating the oxidation of phytohormones like indole-3-acetic acid, propylene can influence various growth responses in plants, potentially affecting processes such as cell elongation and division.

Pharmacokinetics

Information on the pharmacokinetics of propylene in humans is not well-documented, as its primary uses are industrial and agricultural. Its metabolism may be influenced by environmental factors, and its effects are primarily studied in the context of plant biology rather than human pharmacology.

Dosage

Children: Refer to specific drug formulations and product labels as purified substances can vary widely in their use and dosing.

Adults: Refer to specific drug formulations and product labels as purified substances can vary widely in their use and dosing.

Mechanism of action

The mechanism of action for purified compounds varies widely depending on the specific substance. Generally, purified drugs exert their effects by interacting with specific biological targets, such as receptors, enzymes, or ion channels, leading to a desired therapeutic effect. This interaction can involve binding to receptors to activate or inhibit signaling pathways, modulating enzymatic activity, or altering physiological processes.

Pharmacodynamics

Pharmacodynamics describes the effects of a drug on the body and the relationship between drug concentration and effect. For purified drugs, this can involve dose-response relationships and the time course of their action. The purified form often enhances potency and reduces variability in response among patients, which can lead to more predictable therapeutic outcomes. The overall effect is determined by the drug's affinity for its target, the efficacy of the drug-receptor interaction, and the downstream signaling pathways activated as a result of this interaction.

Pharmacokinetics

Pharmacokinetics involves the absorption, distribution, metabolism, and excretion (ADME) of a drug. For purified substances, absorption can be more efficient due to the absence of impurities that may affect solubility or stability. Distribution may also be enhanced, leading to higher bioavailability. Metabolism can be influenced by the structure of the purified compound, as it may be metabolized more readily by liver enzymes. Excretion typically occurs through the kidneys or liver, depending on the molecular characteristics of the purified drug.

Pregnancy

Consult with a healthcare professional, as the safety of purified forms of medications during pregnancy may vary depending on the specific substance.

Breast-feeding

Consult with a healthcare professional, as the safety of purified forms of medications during breastfeeding may vary depending on the specific substance.

Storage

Store in a cool, dry place, away from light and moisture, and keep out of reach of children.

Dosage

Children: Refer to established guidelines for exposure and toxicity management as there is no standard dosing for therapeutic use.

Adults: Refer to established guidelines for exposure and toxicity management as there is no standard dosing for therapeutic use.

Mechanism of action

Toluene exerts its effects primarily through the central nervous system. It acts as a non-specific CNS depressant, interfering with neurotransmitter systems and causing disruption in synaptic transmission. Toluene is known to enhance the inhibitory effects of GABA (gamma-aminobutyric acid) and may inhibit NMDA (N-methyl-D-aspartate) receptors, contributing to its sedative effects.

Pharmacodynamics

The pharmacodynamic effects of toluene include sedation, euphoria, and decreased cognitive and motor functions. Due to its lipophilic nature, toluene readily crosses the blood-brain barrier, leading to central nervous system effects. Toxicological effects can include headaches, dizziness, ataxia, and, in severe cases, unconsciousness or coma. Chronic exposure can lead to neurotoxicity and cognitive deficits.

Pharmacokinetics

Toluene is rapidly absorbed through inhalation, as well as through the gastrointestinal tract and skin. It is widely distributed in body tissues, particularly in lipid-rich organs like the brain and adipose tissue. Metabolism occurs primarily in the liver via cytochrome P450 enzymes, leading to the formation of various metabolites, including benzyl alcohol and benzoic acid. Excretion occurs mainly through urine, with a half-life that can vary depending on the route of exposure and individual factors.

Adverse effects

• Headache
• Dizziness
• Nausea
• Vomiting
• Central nervous system depression
• Respiratory irritation
• Dermatitis
• Liver damage
• Kidney damage
• Hearing loss

Precautions

• Use with caution in patients with a history of substance abuse
• Avoid exposure in patients with respiratory diseases
• Handle with care in pregnant women due to potential teratogenic effects
• Ensure adequate ventilation when using toluene

Pregnancy

Toluene is classified as a teratogen and can cause developmental issues in the fetus if exposure occurs during pregnancy. Caution is advised.

Breast-feeding

Toluene can be excreted in breast milk. Caution is advised for nursing mothers to avoid exposure.

Storage

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

Formulations

• Solvent
• Aerosol spray
• Adhesives
• Paint thinners

Indications

• Asthma
• Allergic rhinitis
• Rheumatoid arthritis
• Systemic lupus erythematosus
• Dermatitis
• Psoriasis
• Inflammatory bowel disease

Dosage

Children: Refer to BNF for Children for specific dosing recommendations based on condition and formulation.

Adults: Refer to BNF for specific dosing recommendations based on condition and formulation.

Mechanism of action

Triamcinolone inhibits phospholipase A2 on cell membranes, preventing the breakdown of lysosomal membranes of leukocytes. This action reduces the formation of arachidonic acid, leading to decreased expression of cyclooxygenase and lipoxygenase, which inhibits the synthesis of prostaglandins and leukotrienes. Additionally, triamcinolone inhibits nuclear factor kappa-B, reducing pro-inflammatory signals such as interleukin-6 and interleukin-8. It interacts with specific intracellular receptor proteins to alter the expression of corticosteroid-responsive genes, leading to the synthesis of proteins like lipocortin that further inhibit inflammatory pathways.

Pharmacodynamics

Triamcinolone exhibits significant anti-inflammatory effects through multiple mechanisms, including suppression of immune cell migration and modulation of inflammatory mediator production. Its effects can lead to reduced edema, erythema, and pain associated with inflammatory processes. The drug’s action is mediated by its ability to influence gene expression in target tissues, resulting in a broad range of effects on the immune response and inflammation.

Pharmacokinetics

Triamcinolone is well absorbed following parenteral administration, with peak plasma concentrations typically observed within a few hours. It has a relatively long half-life, which allows for sustained therapeutic effects. The drug is metabolized primarily in the liver and excreted via the kidneys. Its pharmacokinetic profile may vary depending on the route of administration and the specific formulation used.

Interactions

• mitotane+triamcinolone: Moderate (decreases exposure)
• rifampicin+triamcinolone: Moderate (decreases exposure)
• cobicistat+triamcinolone: Unknown (increases exposure)
• idelalisib+triamcinolone: Unknown (increases exposure)
• clarithromycin+triamcinolone: Unknown (increases exposure)

Pregnancy

Corticosteroids, including triamcinolone, should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. They may cause fetal harm, particularly when used in high doses or for prolonged periods in the second and third trimesters.

Breast-feeding

Triamcinolone is excreted in human milk, and caution should be exercised when administering to nursing mothers. The benefits of breastfeeding should be weighed against the potential risk of adverse effects on the infant.

Storage

Store at room temperature, away from light and moisture. Do not freeze.

Mechanism of action

Ethylene glycol is metabolized by alcohol dehydrogenase to glycoaldehyde, which is then metabolized to glycolic, glyoxylic, and oxalic acids. These acids, along with excess lactic acid are responsible for the anion gap metabolic acidosis. Oxalic acid readily precipitates with calcium to form insoluble calcium oxalate crystals. Tissue injury is caused by widespread deposition of oxalate crystals and the toxic effects of glycolic and glyoxylic acids.

Mechanism of action

Acute poisoning ... is related to ... inhibiting action on enzyme acetylcholinesterase. Toxic manifestations generally occur only after more than 50% of plasma cholinesterase is inhibited. ... Methyl parathion ... depend on oxidative activation by replacement of thiono-sulfur with oxygen for ... toxicity. Methyl parathion has only a slight inhibitory action on acetylcholinesterase and butyrylcholinesterase, but its active metabolite, methyl paraoxon, is a potent inhibitor of both these enzymes. A study was conducted examining the inhibition of (Ca2+ and Mg2+)-ATPase by parathion (56382) and methyl parathion. Enzyme activity was assessed spectrophotometrically in pig erythrocyte membranes containing calcium2+ (Ca2+) and magnesium2+ and in solubilized membrane preparations incubated with the test agents. The enzyme response to ATP was biphasic. Equations expressing the kinetics of the substrate curves described two classes of the ATP binding active site, one with high affinity and low maximum rate and one with low affinity and high maximum rate. High affinity active sites were stimulated by low ATP concentrations (20 uM), whereas low affinity active sites were stimulated by high ATP levels (2 mM). Parathion and methylparathion dose dependently inhibited enzyme activity; parathion had a greater inhibitory effect than methylparathion. Lineweaver-Burke and Dixon plots indicated noncompetitive inhibition. Parathion and methylparathion induced enzyme inhibition occurred over a range of free calcium ion concentrations (0.5 to 5 mM); the inhibition was significantly greater at lower Ca2+ concentrations (1 to 100 uM) than at higher concentrations. The authors conclude that parathion and methylparathion inhibit ATPase activity by binding to a site on the enzyme rather than through an interaction with associated lipids. For more Mechanism of Action (Complete) data for METHYL PARATHION (6 total), please visit the HSDB record page.

Mechanism of action

In an in vitro study of the mechanism of action of ethylene as a plant growth inhibitor, the effects of ethylene and some of its analogs, including propylene, on the oxidation of indole-3-acetic acid were examined. Ethylene and its analogs inhibited the oxidation of indole-3-acetic acid by peroxidase under conditions where the iron complex (compound III, an oxy-ferrous complex of peroxidase) shuttle was activated. Inhibition occurred only in the presence of the superoxide anion radical 02(-). Spectral and kinetic data indicated that ethylene and its analogs enhanced the rate of reaction of 02(-) with peroxidase; ie, the iron complex (compound III) shuttle, resulting in the formation of compound III. Propylene was a less effective inhibitor than ethylene.

Mechanism of action

Corticosteroids like triamcinolone inhibit phospholipase A2 on cell membranes, preventing the breakdown of lysosomal membranes of leukocytes, which in turn prevent the formation of arachidonic acid, which decrease expression of cyclooxygenase and lipoxygenase, inhibiting synthesis of prostaglandins and leukotrienes. Anti-inflammatory activity occurs via reversal of vascular dilation and reducing permeability, which prevents macrophage and leukocyte migration. Triamcinolone also inhibits nuclear factor kappa-B, which decreases the production of pro-inflammatory signals such as interleukin-6, interleukin-8, and monocyte chemoattractant protein-1. Glucocorticoids are capable of suppressing the inflammatory process through numerous pathways. They interact with specific intracellular receptor proteins in target tissues to alter the expression of corticosteroid-responsive genes. Glucocorticoid-specific receptors in the cell cytoplasm bind with steroid ligands to form hormone-receptor complexes that eventually translocate to the cell nucleus. There these complexes bind to specific DNA sequences and alter their expression. The complexes may induce the transcription of mRNA leading to synthesis of new proteins. Such proteins include lipocortin, a protein known to inhibit PLA2a and thereby block the synthesis of prostaglandins, leukotrienes, and PAF. Glucocorticoids also inhibit the production of other mediators including AA metabolites such as COX, cytokines, the interleukins, adhesion molecules, and enzymes such as collagenase. /Glucocorticoids/ Corticosteroids diffuse across cell membranes and complex with specific cytoplasmic receptors. These complexes then enter the cell nucleus, bind to DNA (chromatin), and stimulate transcription of messenger RNA (mRNA) and subsequent protein synthesis of various inhibitory enzymes responsible for the anti-inflammatory effects of topical corticosteroids. These anti-inflammatory effects include inhibition of early processes such as edema, fibrin deposition, capillary dilatation, movement of phagocttes into the area, and phagocytic activities. Later processes, such as capillary production, collagen deposition, and keloid formation also are inhibited by corticosteroids. The overall actions of topical corticosteroids are catabolic. /Corticosteroids (topical)/ The potent anti-inflammatory action may be due to an inhibition of the secretion of growth factors, endothelial activating and other cytokines from lymphocytes, eosinophils, macrophages, fibroblasts, and mast cells. The results are decreased influx of inflammatory cells into the bronchial walls, due in part to inhibition of expression of adhesion molecules on the endothelium and in the tissue. Decreased activation and survival of eosinophils in the lung tissue and a reduction in numbers of mast cells are further effects. Corticosteroids may inhibit release of mediators from basophils and enzymes from macrophages. There is decreased permeability through vasoconstriction and direct inhibition of endothelial cell contradiction. Beta-adrenergic-receptor numbers may be increased, which results in an enhanced response to beta-adrenergic bronchodilators and reduced down-regulation of beta-receptors after prolonged beta-agonist exposure. Inhaled corticosteroids also inhibit mucus secretion in airways, possibly by a direct action on submucosal gland cells and an indirect inhibitory effect caused by the reduction in inflammatory mediators that stimulate mucus secretion. The amount and viscosity of sputum are reduced. /Corticosteroids (inhalation-local/

Pharmacodynamics

Triamcinolone is a corticosteroid with anti-inflammatory properties. These properties are used to treat inflammation in conditions that affect various organs and tissues. Triamcinolone should not be administered as an epidural injection.