COCCIMED PLUS POWDER

Indications

• Thickening agent in topical formulations
• Anti-caking agent in powders
• Carrier for active pharmaceutical ingredients

Dosage

Children: Refer to specific formulation guidelines in the BNF for Children.

Adults: Refer to specific formulation guidelines in the BNF.

Mechanism of action

Aerosil exerts its effects primarily through its surface characteristics. The interaction of silica particles with biological systems can lead to cytotoxicity and cellular transformation, which are influenced by the distribution of silanol groups and the presence of trace metals such as iron. The cytotoxic effects are related to the ability of silica to generate reactive oxygen species, leading to oxidative stress in cells. The biological response to aerosil is sensitive to the composition and structural features of the silica surface, indicating that its activity is a surface-originated phenomenon.

Pharmacodynamics

The pharmacodynamic properties of aerosil are related to its ability to modify the rheological properties of formulations, improve flowability, and prevent clumping. Its cytotoxic effects at high concentrations can lead to cellular stress and transformation, although these effects are primarily of concern in occupational exposure rather than therapeutic use. The dose-response relationship can vary based on the specific type of silica and its surface modifications.

Pharmacokinetics

Aerosil is not absorbed systemically when used in pharmaceutical formulations due to its high molecular weight and physical properties. Inhalation of silica dust can lead to pulmonary exposure, where it may elicit inflammatory responses and potentially lead to silicosis over prolonged exposure. Its elimination from the body does not occur via typical metabolic pathways; instead, silica particles may be cleared from the lungs by macrophage action and mucociliary clearance mechanisms.

Indications

• Coccidiosis in poultry
• Coccidiosis in livestock
• Prevention of coccidial infections in animals

Dosage

Children: Refer to veterinary guidelines for specific dosing for younger animals, as it may vary according to weight and age.

Adults: Refer to veterinary guidelines for specific dosing based on the type of animal and severity of infection.

Mechanism of action

Amprolium acts as a thiamine antagonist, inhibiting the uptake of thiamine in the protozoa. This leads to depletion of thiamine within the parasites, which is essential for their energy metabolism and growth. The lack of thiamine disrupts several metabolic pathways, ultimately resulting in the death of the parasitic organisms.

Pharmacodynamics

Amprolium exhibits selective toxicity towards protozoa by exploiting the differences in thiamine metabolism between the host and the parasite. The drug's action is primarily coccidiostatic, preventing the development and reproduction of Eimeria species. The effectiveness of amprolium is influenced by factors such as the specific strain of Eimeria, the dosage administered, and the duration of treatment.

Pharmacokinetics

Amprolium is well absorbed after oral administration, with peak plasma concentrations occurring within a few hours. It is primarily metabolized in the liver, and its metabolites are excreted mainly through the urine. The drug has a relatively short half-life, necessitating multiple doses for effective treatment. The pharmacokinetic profile may vary between species, and veterinary guidelines should be followed for specific dosing regimens.

Adverse effects

• Anorexia
• Weight loss
• Neurological signs including ataxia
• Thiamine deficiency symptoms

Precautions

• Use with caution in animals with pre-existing neurological conditions
• Monitor for signs of thiamine deficiency

Pregnancy

There are no adequate and well-controlled studies in pregnant animals. Use with caution.

Breast-feeding

Not established. Caution is advised.

Storage

Store in a cool, dry place, away from light.

Formulations

• Oral powder
• Oral solution

Indications

• Hypoglycemia
• Caloric supplementation in patients unable to eat
• Fluid replacement therapy
• Parenteral nutrition

Dosage

Children: Paediatric doses must be determined based on clinical condition and specific needs. Refer to the BNF for Children for appropriate dosing information.

Adults: The dosage of dextrose in adults varies based on clinical condition and route of administration. For hypoglycemia, intravenous dextrose 50% (D50W) is commonly administered. Refer to the BNF for specific dosing guidelines.

Mechanism of action

Dextrose supplies energy to tissues by generating ATP and NADH through glycolysis, where glucose is phosphorylated by hexokinase to form glucose 6-phosphate. This activates glucose for breakdown, ultimately converting glucose into energy molecules. Dextrose also plays a role in gene transcription, enzyme activity, and hormone secretion, regulating glucose homeostasis and cellular metabolic integrity.

Pharmacodynamics

Blood glucose acts as a crucial energy source for cellular activities and functions as a signaling molecule. It is oxidized into carbon dioxide and water, producing energy through glycolysis, the citric cycle, and oxidative phosphorylation. Dextrose can be converted into fat for energy storage and is stored as glycogen in the liver and muscles. Its administration, particularly orally, enhances insulin secretion due to stimulation of incretin hormones.

Pharmacokinetics

Dextrose is rapidly absorbed in the gastrointestinal tract, leading to a quick elevation of blood glucose levels. It is distributed throughout the body and can be utilized by various tissues for energy. The metabolism of dextrose primarily occurs in the liver, where it can be stored as glycogen or converted into fat. Renal excretion may occur when blood glucose levels are excessively high.

Adverse effects

• Hyperglycemia
• Fluid overload
• Hypokalemia
• Thrombophlebitis at injection site

Interactions

• Corticosteroids may increase blood glucose levels
• Beta-blockers may mask symptoms of hypoglycemia
• Diuretics may cause electrolyte imbalances

Precautions

• Use with caution in patients with diabetes mellitus
• Monitor blood glucose levels regularly
• Use cautiously in patients with renal impairment or heart failure

Pregnancy

Dextrose is generally considered safe for use during pregnancy when clinically indicated, but should be used with caution.

Breast-feeding

Dextrose can be used during breastfeeding as it is a natural sugar found in breast milk.

Storage

Store at room temperature, away from direct sunlight, and protect from freezing.

Formulations

• Dextrose 5% solution for infusion
• Dextrose 10% solution for infusion
• Dextrose 50% solution for injection
• Oral dextrose tablets

Indications

• Food preservation
• Antioxidant in pharmaceutical formulations
• Reducing agent in chemical processes
• Component in certain injectable medications

Dosage

Children: Refer to the specific product information or clinical guidelines for dosing recommendations, as dosages can vary based on formulation and intended use.

Adults: Refer to the specific product information or clinical guidelines for dosing recommendations, as dosages can vary based on formulation and intended use.

Mechanism of action

Metabisulphite acts as a reducing agent through its ability to donate electrons, leading to the reduction of other compounds. It reacts with free radicals and other reactive species, thus preventing oxidative damage to cells and tissues. The sulfite ion can also interact with thiol groups in proteins, altering their structure and function, which can have both beneficial and adverse effects depending on the context.

Pharmacodynamics

The pharmacodynamics of metabisulphite involve its antioxidant properties, which help protect cells from oxidative stress. By scavenging free radicals, it contributes to the stabilization of various compounds, prolonging their efficacy. However, its potential to induce oxidative stress and trigger allergic reactions in susceptible individuals is also recognized, necessitating caution in its use.

Pharmacokinetics

Metabisulphite is rapidly absorbed when administered, and its pharmacokinetic profile is influenced by the route of administration. It is metabolized to sulfite and further to sulfate in the liver. The elimination half-life is relatively short, with renal excretion being the primary route of elimination. Individuals with compromised renal function may have altered clearance rates, requiring careful monitoring.

Contra-indications

• Hypersensitivity to metabisulfite or any other sulfite compounds
• Asthma or a history of sulfite sensitivity

Adverse effects

• Allergic reactions, including anaphylaxis
• Respiratory distress in sensitive individuals
• Skin reactions such as rashes or urticaria

Interactions

• May interact with certain medications that can cause allergic reactions
• Possible enhancement of the effects of other sulfite-containing medications

Precautions

• Use with caution in patients with asthma or sulfite sensitivity
• Monitor for respiratory reactions in susceptible individuals

Pregnancy

Safety during pregnancy has not been established; use only if clearly needed.

Breast-feeding

Safety during breastfeeding is not well established; use with caution.

Storage

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

Formulations

• Powder for solution
• Tablet form
• Inhalation solution

Indications

• Bacterial infections in veterinary medicine
• Coccidiosis in poultry
• Treatment of certain protozoal infections

Dosage

Children: Refer to the relevant prescribing information for specific dosing guidelines as per clinical condition.

Adults: Refer to the relevant prescribing information for specific dosing guidelines as per clinical condition.

Mechanism of action

Sulfaquinoxaline acts as a competitive antagonist of para-aminobenzoic acid (PABA), a key substrate in the bacterial synthesis of folic acid. By inhibiting the enzyme dihydropteroate synthase, sulfaquinoxaline prevents the incorporation of PABA into dihydropteroic acid, which is the precursor of folic acid. This inhibition disrupts the formation of folic acid necessary for DNA synthesis, thus hindering bacterial cell multiplication. Mammalian cells, which utilize preformed folic acid, are not affected by this mechanism.

Pharmacodynamics

The pharmacodynamics of sulfaquinoxaline are characterized by its ability to inhibit bacterial growth through the blockade of folic acid synthesis. It demonstrates a bacteriostatic effect, meaning it stops bacteria from multiplying rather than killing them directly. The efficacy of sulfaquinoxaline depends on the susceptibility of the bacteria involved and is influenced by the presence of PABA in the environment, which can compete with the drug.

Pharmacokinetics

Sulfaquinoxaline is well absorbed from the gastrointestinal tract and achieves therapeutic levels in the serum. It has a distribution that allows it to penetrate tissues and body fluids. The drug is metabolized in the liver and excreted primarily through the kidneys. The pharmacokinetic profile can be influenced by factors such as the presence of other substances that may compete for absorption or metabolism.

Contra-indications

• Hypersensitivity to sulfonamides
• Severe hepatic or renal impairment
• Porphyria

Adverse effects

• Allergic reactions including rash, itching, and fever
• Gastrointestinal disturbances such as nausea and vomiting
• Hematological effects including leukopenia, thrombocytopenia, and aplastic anemia
• Kernicterus in newborns
• Crystalluria

Interactions

• May enhance the effects of anticoagulants such as warfarin
• Potentially decreases the effectiveness of oral contraceptives
• Can increase the toxicity of methotrexate
• May interact with other drugs that affect renal function

Precautions

• Use with caution in patients with renal impairment
• Monitor for signs of blood dyscrasias
• Adequate hydration is important to prevent crystalluria
• Caution in patients with a history of asthma or allergic reactions

Pregnancy

Use during pregnancy only if clearly needed, as sulfonamides can cross the placenta and may cause harm to the fetus.

Breast-feeding

Breastfeeding is not recommended while taking sulfaquinoxaline due to potential adverse effects on the infant.

Storage

Store at room temperature, away from moisture and heat.

Formulations

• Tablets
• Suspensions
• Injectable forms

Indications

• Vitamin deficiency syndromes (e.g., scurvy for vitamin C deficiency, rickets for vitamin D deficiency)
• Support for immune function
• Antioxidant support
• Bone health maintenance
• Vision health
• Energy metabolism support

Dosage

Children: Refer to the BNF for Children for specific vitamin dosing guidelines, which depend on age and nutritional requirements.

Adults: Refer to specific vitamin guidelines as dosage varies significantly depending on the type of vitamin and individual needs.

Mechanism of action

Vitamins function primarily as coenzymes or precursors for coenzymes in enzymatic reactions. For instance, B vitamins are involved in energy metabolism, while vitamins A, C, D, E, and K support various physiological functions including vision, antioxidant activity, calcium regulation, and blood clotting. Each vitamin has a unique mechanism of action based on its structure and role in the body.

Pharmacodynamics

Vitamins exert their effects at the cellular level, influencing metabolic pathways, gene expression, and immune responses. For example, vitamin D regulates calcium and phosphate homeostasis, while vitamin A is crucial for vision and immune function. Deficiencies in vitamins can lead to a range of disorders, highlighting their importance in maintaining health.

Pharmacokinetics

The pharmacokinetics of vitamins vary widely. Fat-soluble vitamins (A, D, E, and K) are stored in liver and adipose tissues and can be released into circulation as needed. Water-soluble vitamins (B-complex and C) are not stored and must be consumed regularly, with excess amounts excreted in urine. Absorption rates, half-lives, and distribution can also differ based on the specific vitamin and individual metabolic factors.

Interactions

• tretinoin+vitamin: Severe (increases risk of vitamin toxicity)
• retinoids+vitamin: Severe (increases risk of vitamin toxicity)
• retinoids+vitamin: Moderate (increases risk of toxicity)
• carbamazepine+vitamin: Unknown (decreases effects)
• cobicistat+vitamin: Unknown (increases exposure)
• vitamin D substances+digoxin: Unknown (increases risk of toxicity)
• idelalisib+vitamin: Unknown (increases exposure)
• clarithromycin+vitamin: Unknown (increases exposure)

Pregnancy

Consult healthcare professional before use. Vitamin supplementation during pregnancy should be carefully managed to avoid hypervitaminosis.

Breast-feeding

Consult healthcare professional before use. Some vitamins can pass into breast milk and may affect the infant.

Storage

Store in a cool, dry place, away from direct sunlight. Ensure it is kept out of reach of children.

Formulations

• {'name': 'Vitamin A', 'form': 'Capsule', 'strength': '10000 IU'}
• {'name': 'Vitamin D', 'form': 'Tablet', 'strength': '1000 IU'}
• {'name': 'Vitamin E', 'form': 'Softgel', 'strength': '400 IU'}

Mechanism of action

...Some quartz and cristobalite dusts (crystalline) as well as the diatomaceous earths (amorphous), but not the pyrogenic amorphous silica, were cytotoxic and induced morphological transformation of SHE cells in a concentration-dependent manner. The ranking in cytotoxicity was different from that in transforming potency, suggesting two separate molecular mechanisms for the two effects. The cytotoxic and transforming potencies were different from one dust to another, even among the same structural silicas. The type of crystalline structure (quartz vs cristobalite) and the crystalline vs biogenic amorphous form did not correlate with cytotoxic or transforming potency of silica dusts. Comparison of cellular effects induced by original and surface modified samples revealed that several surface functionalities modulate cytotoxic and transforming potencies. The cytotoxic effects appeared to be related to the distribution and abundance of silanol groups and to the presence of trace amounts of iron on the silica surface. Silica particles with fractured surfaces and/or iron-active sites, able to generate reactive oxygen species, induced SHE cell transformation. The results show that the activity of silica at the cellular level is sensitive to the composition and structure of surface functionalities and confirm that the biological response to silica is a surface originated phenomenon. In vivo exposure of rat lungs to crystalline silica either by intratracheal instillation or by inhalation results in an increase in mRNA levels for inducible nitric oxide synthase (iNOS) in bronchoalveolar lavage cells (BALC), elevated nitric oxide (.NO) production by BALC, and an increase in .NO-dependent chemiluminescence (CL) from alveolar macrophages (AM). Induction of iNOS message occurs in both AM and polymorphonuclear leukocytes (PMN) harvested from silica-exposed lungs but is not significantly elevated in lavaged lung tissue. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by summarizing results of in vitro, animal, and human investigations. These results support four basic mechanisms in the etiology of CWP and silicosis: a) direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring; b) activation of oxidant production by pulmonary phagocytes, which overwhelms the antioxidant defenses and leads to lipid peroxidation, protein nitrosation, cell injury, and lung scarring; c) activation of mediator release from alveolar macrophages and epithelial cells, which leads to recruitment of polymorphonuclear leukocytes and macrophages, resulting in the production of proinflammatory cytokines and reactive species and in further lung injury and scarring; d) secretion of growth factors from alveolar macrophages and epithelial cells, stimulating fibroblast proliferation and eventual scarring. Results of in vitro and animal studies provide a basis for proposing these mechanisms for the initiation and progression of pneumoconiosis. Data obtained from exposed workers lend support to these mechanisms. /The authors/ reported previously that freshly fractured silica (FFSi) induces activator protein-1 (AP-1) activation through extracellular signal-regulated protein kinases (ERKs) and p38 kinase pathways. In the present study, the biologic activities of FFSi and aged silica (ASi) were compared by measuring their effects on the AP-1 activation and phosphorylation of ERKs and p38 kinase. The roles of reactive oxygen species (ROS) in this silica-induced AP-1 activation were also investigated. FFSi-induced AP-1 activation was four times higher than that of ASi in JB6 cells. FFSi also caused greater phosphorylation of ERKs and p38 kinase than ASi. FFSi generated more ROS than ASi when incubated with the cells as measured by electron spin resonance (ESR). Studies using ROS-sensitive dyes and

Mechanism of action

Glucose supplies most of the energy to all tissues by generating energy molecules ATP and NADH during a series of metabolism reactions called glycolysis. Glycolysis can be divided into two main phases where the preparatory phase is initiated by the phosphorylation of glucose by hexokinase to form glucose 6-phosphate. The addition of the high-energy phosphate group activates glucose for the subsequent breakdown in later steps of glycolysis and is the rate-limiting step. Products end up as substrates for following reactions, to ultimately convert C6 glucose molecule into two C3 sugar molecules. These products enter the energy-releasing phase where the total of 4ATP and 2NADH molecules are generated per one glucose molecule. The total aerobic metabolism of glucose can produce up to 36 ATP molecules. These energy-producing reactions of glucose are limited to D-glucose as L-glucose cannot be phosphorylated by hexokinase. Glucose can act as precursors to generate other biomolecules such as vitamin C. It plays a role as a signaling molecule to control glucose and energy homeostasis. Glucose can regulate gene transcription, enzyme activity, hormone secretion, and the activity of glucoregulatory neurons. The types, number, and kinetics of glucose transporters expressed depends on the tissues and fine-tunes glucose uptake, metabolism, and signal generation to preserve cellular and whole body metabolic integrity. Vascular calcification is a hallmark of type 2 diabetes. Glucose stimulates calcification in culture of vascular smooth muscle cells (VSMCs) but the underlying mechanisms remain obscure. We observed that high glucose levels stimulated mouse and human VSMC trans-differentiation into chondrocytes, with increased levels of Sox9, type II collagen, glycosaminoglycan and Runx2 expression, and increased alkaline phosphatase activity and mineralization. These effects were associated with increased expression of IL-1beta, which stimulated alkaline phosphatase and calcification, suggesting that glucose induces chondrocyte differentiation of VSMCs, possibly through IL-1beta activation.

Pharmacodynamics

Blood glucose is an obligatory energy source for humans involved in various cellular activities, and it also acts as a signaling molecule for diverse glucose-sensing molecules and proteins. Glucose undergoes oxidation into carbon dioxide, water, and yields energy molecules in the process of glycolysis and subsequent citric cycle and oxidative phosphorylation. Glucose is readily converted into fat in the body which can be used as a source of energy as required. Under a similar conversion into storage of energy, glucose is stored in the liver and muscles as glycogen. Glucose stores are mobilized in a regulated manner, depending on the tissues' metabolic demands. Oral glucose tablets or injections serve to increase the supply of glucose and oral glucose administration is more effective in stimulating insulin secretion because it stimulates the incretin hormones from the gut, which promotes insulin secretion.

Mechanism of action

Bacteriostatic. Sulfonamides interfere with the biosynthesis of folic acid in bacterial cells; they compete with paraaminobenzoic acid (PABA) for incorporation in the folic acid molecule. By replacing the PABA molecule and preventing the folic acid formation required for DNA synthesis, the sulfonamides prevent multiplication of the bacterial cell. Susceptible organisms must synthesize their own folic acid; mammalian cells use preformed folic acid and, therefore, are not susceptible. Cells that produce excess PABA or environments with PABA, such as necrotic tissues, allow for resistance by competition with the sulfonamide. /Sulfonamides/ Sulfonamides are structural analogs and competitive antagonists of para-aminobenzoic acid (PABA) and thus prevent normal bacterial utilization of PABA for the synthesis of folic acid (pteroylglutamic acid). More specifically, sulfonamides are competitive inhibitors of dihydropteroate synthase,the bacterial enzyme responsible for the incorporation of PABA into dihydropteroic acid, the immediate precursor of folic acid. Sensitive microorganisms are those that must synthesize their own folic acid; bacteria that can utilize preformed folate are not affected. Bacteriostasis induced by sulfonamides is counteracted by PABA competitively. Sulfonamides do not affect mammalian cells by this mechanism, since they require preformed folic acid and cannot synthesize it. /Sulfonamides/