Diclofenac sodium, Tobramycin
Indications
Diclofenac sodium, Tobramycin is used for:
DICLOFENAC
For the acute and chronic treatment of signs and symptoms of osteoarthritis and rheumatoid arthritis
TOBRAMYCIN
For the treatment of pseudomonas aeruginosa lung infections. Also being investigated for use in the treatment of sinus infections
For the acute and chronic treatment of signs and symptoms of osteoarthritis and rheumatoid arthritis
TOBRAMYCIN
For the treatment of pseudomonas aeruginosa lung infections. Also being investigated for use in the treatment of sinus infections
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Diclofenac sodium, Tobramycin :
Mechanism of Action
DICLOFENAC
The antiinflammatory effects of diclofenac are believed to be due to inhibition of both leukocyte migration and the enzyme cylooxygenase (cox-1 and cox-2), leading to the peripheral inhibition of prostaglandin synthesis. As prostaglandins sensitize pain receptors, inhibition of their synthesis is responsible for the analgesic effects of diclofenac. Antipyretic effects may be due to action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat dissipation
TOBRAMYCIN
Tobramycin binds irreversibly to one of two aminoglycoside binding sites on the 30 s ribosomal subunit, inhibiting bacterial protein synthesis. Tobramycin may also destabilize bacterial memebrane by binding to 16 s 16 s r-rna. An active transport mechanism for aminoglycoside uptake is necessary in the bacteria in order to attain a significant intracellular concentration of tobramycin
The antiinflammatory effects of diclofenac are believed to be due to inhibition of both leukocyte migration and the enzyme cylooxygenase (cox-1 and cox-2), leading to the peripheral inhibition of prostaglandin synthesis. As prostaglandins sensitize pain receptors, inhibition of their synthesis is responsible for the analgesic effects of diclofenac. Antipyretic effects may be due to action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat dissipation
TOBRAMYCIN
Tobramycin binds irreversibly to one of two aminoglycoside binding sites on the 30 s ribosomal subunit, inhibiting bacterial protein synthesis. Tobramycin may also destabilize bacterial memebrane by binding to 16 s 16 s r-rna. An active transport mechanism for aminoglycoside uptake is necessary in the bacteria in order to attain a significant intracellular concentration of tobramycin