TRIAMACORT

Indications

• Dry eye conditions
• Keratoconjunctivitis sicca
• Unstable tear film

Dosage

Children: Apply 3–4 times a day or when required to the eye.

Adults: Apply 3–4 times a day or when required to the eye.

Mechanism of action

Carmellose sodium acts as a viscosity-increasing agent, providing lubrication and hydration. It works by creating a gel-like consistency that mimics natural tears, thus improving moisture retention on the ocular surface. This action alleviates dryness and irritation in the eyes.

Pharmacodynamics

Carmellose sodium exhibits mucomimetic properties, which means it has the ability to mimic natural mucus in the eye. Its effectiveness in reducing symptoms of dryness is attributed to its ability to increase tear film stability and provide a protective barrier against environmental irritants. It does not have systemic effects as it is used topically.

Pharmacokinetics

Carmellose sodium is administered topically and is not absorbed systemically, making its pharmacokinetics primarily local. The onset of action is rapid, providing immediate relief for dry eye symptoms. The duration of action depends on factors such as the formulation and frequency of administration. Due to its high molecular weight, it remains on the ocular surface for an extended period, ensuring prolonged lubrication.

Adverse effects

• Transient blurred vision
• Eye irritation
• Allergic reactions

Precautions

• Consult a healthcare professional if symptoms persist
• Avoid contact with the tip of the dropper to prevent contamination

Pregnancy

Carmellose sodium is generally considered safe for use during pregnancy. However, consult a healthcare provider for personalized advice.

Breast-feeding

Carmellose sodium is not known to pose a risk during breastfeeding, but it is advisable to consult a healthcare provider.

Storage

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

Formulations

• Carmize 0.5% eye drops
• Carmize 1% eye drops
• Cellusan 0.5% eye drops
• Celluvisc 0.5% eye drops
• Liquivisc 0.25% eye gel
• Ocu-Lube Carmellose 0.5% eye drops
• Tearvis 0.5% eye drops

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

• 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

• Bacterial infections
• Pneumonia
• Meningitis
• Syphilis
• Endocarditis
• Skin and soft tissue infections

Dosage

Children: Paediatric dosing for benzylpenicillin is determined by the child's weight and the severity of the infection. Refer to the BNF for Children for specific dosing guidelines.

Adults: The usual adult dose for benzylpenicillin varies based on the type and severity of the infection. It is generally administered via intramuscular or intravenous routes. For severe infections, doses may range from 1 to 4 million units every 4 to 6 hours.

Mechanism of action

Benzylpenicillin exerts its antibacterial effects by inhibiting the synthesis of bacterial cell walls. It binds to penicillin-binding proteins (PBPs) located inside the bacterial cell wall, disrupting the transpeptidation process, which is crucial for cross-linking peptidoglycan layers. This inhibition leads to cell lysis and death of the bacteria.

Pharmacodynamics

Benzylpenicillin demonstrates time-dependent bactericidal activity, meaning its effectiveness is related to the duration of time the drug concentration remains above the minimum inhibitory concentration (MIC) for the target bacteria. It has a narrow spectrum of activity, primarily targeting Gram-positive cocci and some Gram-negative rods.

Pharmacokinetics

Benzylpenicillin is typically administered parenterally due to poor oral absorption. It is rapidly distributed throughout the body and can penetrate various tissues, including the central nervous system during inflammation. The drug is primarily eliminated by renal excretion, with a half-life of approximately 30 minutes to 1 hour in healthy individuals. Dosage adjustments may be necessary in patients with renal impairment.

Interactions

• leflunomide+benzylpenicillin: Unknown (increases exposure)
• nitisinone+benzylpenicillin: Unknown (increases exposure)
• teriflunomide+benzylpenicillin: Unknown (increases exposure)

Pregnancy

Benzylpenicillin is generally considered safe to use during pregnancy, as it is a penicillin antibiotic and has a long history of use.

Breast-feeding

Benzylpenicillin is excreted in breast milk in small amounts, but it is not expected to have adverse effects on a nursing infant.

Storage

Store in a cool, dry place, protected from light. Reconstituted solutions should be used promptly or stored in a refrigerator and used within a limited time frame.

Formulations

• Benzylpenicillin injection

Indications

• Dry eye syndrome
• Ocular lubrication
• Gastroesophageal reflux disease (GERD)
• Topical applications (as a lubricant or protectant)

Dosage

Children: Refer to specific formulation guidelines for recommended dosages, as doses vary widely depending on the formulation and intended use.

Adults: Refer to specific formulation guidelines for recommended dosages, as doses vary widely depending on the formulation and intended use.

Mechanism of action

Carmellose works by increasing the viscosity of solutions and forming a gel-like consistency when mixed with water. This property allows it to act as a lubricant and protectant, particularly in formulations designed for ocular or gastrointestinal use. The water-binding capacity of carmellose helps to retain moisture in tissues, which can be beneficial in treating dryness.

Pharmacodynamics

The pharmacodynamic properties of carmellose are primarily related to its ability to modify the physical properties of solutions and suspensions. It does not exert specific pharmacological effects but rather enhances the bioavailability and stability of active ingredients in pharmaceutical formulations. Its hydrophilic nature allows it to hold water and improve the consistency of products, thus facilitating drug delivery and absorption.

Pharmacokinetics

Carmellose is not absorbed systemically when administered orally, as it is primarily used as an excipient. It passes through the gastrointestinal tract without significant metabolism. The elimination half-life is not applicable, as it does not enter systemic circulation. Its effects are localized to the site of application or ingestion, where it acts as a bulking agent or thickener.

Adverse effects

• Gastrointestinal discomfort
• Bloating
• Diarrhea

Precautions

• Use with caution in patients with gastrointestinal disorders
• Monitor for hypersensitivity reactions

Pregnancy

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

Breast-feeding

Carmellose is considered safe for use during breastfeeding, but it is recommended to seek advice from a healthcare professional.

Storage

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

Formulations

• Powder
• Tablet
• Capsule
• Suspension

Indications

• Allergic rhinitis
• Common cold
• Sinusitis
• Seasonal allergies
• Nasal congestion

Dosage

Children: Refer to specific product formulations and BNF for Children for appropriate dosing in children, as it varies based on age and weight.

Adults: Refer to specific product formulations for dosing instructions, as they can vary by manufacturer and formulation.

Mechanism of action

The antihistamine component works by blocking histamine H1 receptors, which helps alleviate allergy symptoms such as sneezing, itching, and runny nose. The decongestant acts on adrenergic receptors in the nasal mucosa, causing vasoconstriction and reducing nasal congestion. Analgesic components help relieve pain by inhibiting the synthesis of prostaglandins in the central nervous system.

Pharmacodynamics

The combination of antihistamine and decongestant provides a synergistic effect, offering relief from multiple symptoms associated with colds and allergies. The antihistamine reduces allergic reactions and their symptoms, while the decongestant improves airflow through the nasal passages. The analgesic component alleviates discomfort, enhancing the overall therapeutic effect of the drug.

Pharmacokinetics

Absorption rates can vary based on the specific formulations of the drug. Typically, antihistamines are well absorbed from the gastrointestinal tract, with peak plasma concentrations occurring within 1 to 3 hours. Decongestants may have variable bioavailability depending on the route of administration. Metabolism mainly occurs in the liver, and elimination half-lives can range from a few hours to several hours depending on the specific agents included. Renal excretion plays a significant role in the clearance of these drugs.

Pregnancy

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

Breast-feeding

Data is limited; use caution and consider the potential risks versus benefits.

Storage

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

Indications

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

Dosage

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

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

Mechanism of action

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

Pharmacodynamics

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

Pharmacokinetics

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

Pregnancy

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

Breast-feeding

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

Storage

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

Indications

• Used as an emulsifier in pharmaceutical formulations
• Facilitates the solubilization of hydrophobic drugs
• Commonly included in vaccines to enhance efficacy and stability
• Acts as a stabilizer in food and cosmetic products

Dosage

Children: Refer to specific formulation guidelines for paediatric dosing, as polysorbate 80 is typically used in small amounts as an excipient.

Adults: Refer to specific formulation guidelines for adult dosing, as polysorbate 80 is typically used in small amounts as an excipient.

Mechanism of action

Polysorbate 80 functions by reducing the surface tension between two immiscible phases, such as oil and water. It contains both hydrophilic (water-attracting) and lipophilic (fat-attracting) components, which allows it to stabilize emulsions by preventing the coalescence of dispersed droplets. This mechanism enhances the bioavailability of hydrophobic substances by improving their solubility in aqueous environments.

Pharmacodynamics

As a surfactant, polysorbate 80 can improve the absorption and bioavailability of co-administered drugs by enhancing their solubility. Its ability to modify membrane permeability can also affect drug delivery and release profiles. However, polysorbate 80 is generally considered non-toxic at typical concentrations used in formulations.

Pharmacokinetics

Polysorbate 80 is not extensively absorbed through the gastrointestinal tract and is primarily eliminated through feces. It may undergo limited metabolism, with some hydrolysis occurring in the body. Due to its large molecular weight, it does not readily cross biological membranes. The pharmacokinetics can vary depending on the formulation and administration route, such as oral, intravenous, or topical.

Adverse effects

• Hypersensitivity reactions
• Gastrointestinal disturbances
• Injection site reactions
• Headache

Precautions

• Use with caution in patients with known allergies to polysorbates
• Monitor for hypersensitivity reactions, especially in parenteral formulations

Pregnancy

Polysorbate 80 is generally considered safe for use during pregnancy, but it should be used only if clearly needed.

Breast-feeding

Polysorbate 80 is considered safe during breastfeeding, as it is unlikely to affect the nursing infant.

Storage

Store in a cool, dry place, protected from light. Follow specific manufacturer's storage instructions for formulations.

Formulations

• Injectable solution
• Oral liquid
• Topical cream

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

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

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.