Neomycin (as sulfate), Nystatin, Triamcinolone acetonide

Indications

Neomycin (as sulfate), Nystatin, Triamcinolone acetonide is used for: NEOMYCIN
Topical uses include treatment for superficial eye infections caused by susceptible bacteria (used in combination with other antiinfectives), treatment of otitis externa caused by susceptible bacteria, treatment or prevention of bacterial infections in skin lesions, and use as a continuous short-term irrigant or rinse to prevent bacteriuria and gram negative rod bacteremia in abacteriuric patients with indwelling catheters. May be used orally to treat hepatic encephalopathy, as a perioperative prophylactic agent, and as an adjunct to fluid and electrolyte replacement in the treatment of diarrhea caused to enteropathogenic E. coli (EPEC).
NYSTATIN
For treatment of cutaneous or mucocutaneous mycotic infections caused by Candida species
TRIAMCINOLONE
For the treatment of perennial and seasonal allergic rhinitis.

Adult Dose

Child Dose

Renal Dose

Administration

Contra Indications

Precautions

Pregnancy-Lactation

Interactions

Adverse Effects

Side effects of Neomycin (as sulfate), Nystatin, Triamcinolone acetonide :

Mechanism of Action

NEOMYCIN
Aminoglycosides like neomycin "irreversibly" bind to specific 30S-subunit proteins and 16S rRNA. Specifically neomycin 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.
NYSTATIN
Nystatin exerts its antifungal activity by binding to ergosterol found in fungal cell membranes. Binding to ergosterol causes the formation of pores in the membrane. Potassium and other cellular constituents leak from the pores causing cell death.
TRIAMCINOLONE
The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition of arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Firstly, however, these glucocorticoids bind to the glucocorticoid receptors which translocate into the nucleus and bind DNA (GRE) and change genetic expression both positively and negatively. 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.