Fluocinonide, Gentamicin sulphate
Indications
Fluocinonide, Gentamicin sulphate is used for:
FLUOCINONIDE
A topical anti-inflammatory product for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses
GENTAMICIN
For treatment of serious infections caused by susceptible strains of the following microorganisms: p. Aeruginosa, proteus species (indole-positive and indole-negative), e. Coli, klebsiella-enterobactor-serratia species, citrobacter species and staphylococcus species (coagulase-positive and coagulase-negative)
A topical anti-inflammatory product for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses
GENTAMICIN
For treatment of serious infections caused by susceptible strains of the following microorganisms: p. Aeruginosa, proteus species (indole-positive and indole-negative), e. Coli, klebsiella-enterobactor-serratia species, citrobacter species and staphylococcus species (coagulase-positive and coagulase-negative)
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Fluocinonide, Gentamicin sulphate :
Mechanism of Action
FLUOCINONIDE
Fluocinonide is a potent glucocorticoid steroid used topically as anti-inflammatory agent for the treatment of skin disorders such as eczema. It relieves itching, redness, dryness, crusting, scaling, inflammation, and discomfort. Fluocinonide binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (gre) in the promoter region of the target genes. The dna bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase a2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase a2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. Cyclooxygenase (both cox-1 and cox-2) expression is also suppressed, potentiating the effect. In another words, the two main products in inflammation prostaglandins and leukotrienes are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc. ) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. Like other glucocorticoid agents fluocinolone acetonide acts as a physiological antagonist to insulin by decreasing glycogenesis (formation of glycogen). It also promotes the breakdown of lipids (lipolysis), and proteins, leading to the mobilization of extrahepatic amino acids and ketone bodies. This leads to increased circulating glucose concentrations (in the blood). There is also decreased glycogen formation in the liver
GENTAMICIN
Aminoglycosides like gentamicin "irreversibly" bind to specific 30s-subunit proteins and 16s rrna. Specifically gentamicin binds to four nucleotides of 16s rrna and a single amino acid of protein s12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16s rrna of 30s subunit. This region interacts with the wobble base in the anticodon of trna. This leads to interference with the initiation complex, misreading of mrna so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes
Fluocinonide is a potent glucocorticoid steroid used topically as anti-inflammatory agent for the treatment of skin disorders such as eczema. It relieves itching, redness, dryness, crusting, scaling, inflammation, and discomfort. Fluocinonide binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (gre) in the promoter region of the target genes. The dna bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase a2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase a2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. Cyclooxygenase (both cox-1 and cox-2) expression is also suppressed, potentiating the effect. In another words, the two main products in inflammation prostaglandins and leukotrienes are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc. ) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. Like other glucocorticoid agents fluocinolone acetonide acts as a physiological antagonist to insulin by decreasing glycogenesis (formation of glycogen). It also promotes the breakdown of lipids (lipolysis), and proteins, leading to the mobilization of extrahepatic amino acids and ketone bodies. This leads to increased circulating glucose concentrations (in the blood). There is also decreased glycogen formation in the liver
GENTAMICIN
Aminoglycosides like gentamicin "irreversibly" bind to specific 30s-subunit proteins and 16s rrna. Specifically gentamicin binds to four nucleotides of 16s rrna and a single amino acid of protein s12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16s rrna of 30s subunit. This region interacts with the wobble base in the anticodon of trna. This leads to interference with the initiation complex, misreading of mrna so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes