Hydrocortisone, Oxytetracycline, Nystatin
Indications
Hydrocortisone, Oxytetracycline, Nystatin 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
OXYTETRACYCLINE
Oxytetracycline is indicated for treatment of infections caused by a variety of gram positive and gram negative microorganisms including mycoplasma pneumoniae, pasteurella pestis, escherichia coli, haemophilus influenzae (respiratory infections), and diplococcus pneumoniae
NYSTATIN
For treatment of cutaneous or mucocutaneous mycotic infections caused by candida species
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
OXYTETRACYCLINE
Oxytetracycline is indicated for treatment of infections caused by a variety of gram positive and gram negative microorganisms including mycoplasma pneumoniae, pasteurella pestis, escherichia coli, haemophilus influenzae (respiratory infections), and diplococcus pneumoniae
NYSTATIN
For treatment of cutaneous or mucocutaneous mycotic infections caused by candida species
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Hydrocortisone, Oxytetracycline, Nystatin :
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
OXYTETRACYCLINE
Oxytetracycline inhibits cell growth by inhibiting translation. It binds to the 30s ribosomal subunit and prevents the amino-acyl trna from binding to the a site of the ribosome. The binding is reversible in nature. Oxytetracycline is lipophilic and can easily pass through the cell membrane or passively diffuses through porin channels in the bacterial membrane
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
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
OXYTETRACYCLINE
Oxytetracycline inhibits cell growth by inhibiting translation. It binds to the 30s ribosomal subunit and prevents the amino-acyl trna from binding to the a site of the ribosome. The binding is reversible in nature. Oxytetracycline is lipophilic and can easily pass through the cell membrane or passively diffuses through porin channels in the bacterial membrane
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