Hydrocortisone, Natamycin, Neomycin sulfate
Indications
Hydrocortisone, Natamycin, Neomycin sulfate is used for:
HYDROCORTISONE
For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and crohn's disease
NATAMYCIN
For the treatment of fungal blepharitis, conjunctivitis, and keratitis caused by susceptible organisms including fusarium solani keratitis
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)
For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and crohn's disease
NATAMYCIN
For the treatment of fungal blepharitis, conjunctivitis, and keratitis caused by susceptible organisms including fusarium solani keratitis
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)
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Hydrocortisone, Natamycin, Neomycin sulfate :
Mechanism of Action
HYDROCORTISONE
Hydrocortisone 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. The cyclooxygenase (both cox-1 and cox-2) expression is also suppressed, potentiating the effect. In other 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
NATAMYCIN
Like other polyene antibiotics, natamycin inhibits fungal growth by binding to sterols. Specifically, natamycin binds to ergosterol in the plasma membrane, preventing ergosterol-dependent fusion of vacuoles, as well as membrane fusion and fission. This differs from the mechanism of most other polyene antibiotics, which tend to work by altering fungal membrane permeability instead
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
Hydrocortisone 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. The cyclooxygenase (both cox-1 and cox-2) expression is also suppressed, potentiating the effect. In other 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
NATAMYCIN
Like other polyene antibiotics, natamycin inhibits fungal growth by binding to sterols. Specifically, natamycin binds to ergosterol in the plasma membrane, preventing ergosterol-dependent fusion of vacuoles, as well as membrane fusion and fission. This differs from the mechanism of most other polyene antibiotics, which tend to work by altering fungal membrane permeability instead
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