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Drug-Drug Interactions
No Drug - Drug interactions found in our data. We may lack specific data on this medicine and are actively working to update our database. Consult your doctor for personalized advice
Drug-Drug Interactions
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Drug-Food Interactions
No Drug - Food interactions found in our database. Some may be unknown. Consult your doctor for what to avoid during medication.
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Drug-Diseases Interactions
GENTAMICIN-0.3%W/WOther symptoms and signs involving the digestive system and abdomen
Severe
GENTAMICIN-0.3%W/WMyasthenia gravis and other myoneural disorders
Severe
Drug-Diseases Interactions
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GENTAMICIN-0.3%W/WOther symptoms and signs involving the digestive system and abdomen
Severe
How does the disease interact with Gentlee Cream 20 gm:
Adequate hydration is critical for reducing the risk of oto- and nephrotoxicity associated with aminoglycoside usage. Dehydration should preferably be treated before starting therapy. Fluid status should be continuously maintained in patients who are at risk of dehydration, such as those who have severe and/or prolonged diarrhoea or vomiting. If indications of renal irritation appear during therapy, hydration should be increased as directed, followed by a dose reduction if necessary. If urine flow gradually decreases or azotemia worsens, therapy should be discontinued.
How to manage the interaction:
Dehydration should be corrected prior to initiation of therapy. Fluid status should be monitored closely in patients who may be at risk for dehydration, such as those with severe and/or prolonged diarrhea or vomiting. Therapy should be withdrawn if urinary output decreases progressively or azotemia (elevated levels of urea) increases.
Adequate hydration is critical for reducing the risk of oto- and nephrotoxicity associated with aminoglycoside usage. Dehydration should preferably be treated before starting therapy. Fluid status should be continuously maintained in patients who are at risk of dehydration, such as those who have severe and/or prolonged diarrhoea or vomiting. If indications of renal irritation appear during therapy, hydration should be increased as directed, followed by a dose reduction if necessary. If urine flow gradually decreases or azotemia worsens, therapy should be discontinued.
How to manage the interaction:
Dehydration should be corrected prior to initiation of therapy. Fluid status should be monitored closely in patients who may be at risk for dehydration, such as those with severe and/or prolonged diarrhea or vomiting. Therapy should be withdrawn if urinary output decreases progressively or azotemia (elevated levels of urea) increases.
GENTAMICIN-0.3%W/WMyasthenia gravis and other myoneural disorders
Severe
How does the disease interact with Gentlee Cream 20 gm:
Aminoglycosides can elicit dose-related neuromuscular blockade and muscle weakness, especially in patients with neuromuscular illness or hypocalcemia, as well as in those undergoing general anaesthesia, neuromuscular blocking medications, or substantial transfusions of citrate-anticoagulated blood. Although neuromuscular blockade caused by aminoglycosides is usually self-limiting, it can occasionally result in respiratory paralysis. The most potent neuromuscular blocking drug in the class is regarded to be neomycin. However, the risk is greatest with large dosages instilled intraperitoneally or intrapleurally, or with fast intravenous administration of parenteral aminoglycosides. In patients with neuromuscular problems (e.g., myasthenia gravis, parkinsonian syndrome, botulism) or hypocalcemia, aminoglycoside therapy should be used with caution. If indications of respiratory paralysis appear during aminoglycoside therapy, the medicine should be stopped and, if necessary, mechanical breathing assistance administered.
How to manage the interaction:
Therapy should be administered cautiously in patients with neuromuscular disorders (e.g., myasthenia gravis, Parkinsonian syndrome, botulism) or hypocalcemia (low calcium levels). The drug should be discontinued and mechanical respiratory assistance provided if needed if signs of respiratory paralysis occur during therapy.
Aminoglycosides can elicit dose-related neuromuscular blockade and muscle weakness, especially in patients with neuromuscular illness or hypocalcemia, as well as in those undergoing general anaesthesia, neuromuscular blocking medications, or substantial transfusions of citrate-anticoagulated blood. Although neuromuscular blockade caused by aminoglycosides is usually self-limiting, it can occasionally result in respiratory paralysis. The most potent neuromuscular blocking drug in the class is regarded to be neomycin. However, the risk is greatest with large dosages instilled intraperitoneally or intrapleurally, or with fast intravenous administration of parenteral aminoglycosides. In patients with neuromuscular problems (e.g., myasthenia gravis, parkinsonian syndrome, botulism) or hypocalcemia, aminoglycoside therapy should be used with caution. If indications of respiratory paralysis appear during aminoglycoside therapy, the medicine should be stopped and, if necessary, mechanical breathing assistance administered.
How to manage the interaction:
Therapy should be administered cautiously in patients with neuromuscular disorders (e.g., myasthenia gravis, Parkinsonian syndrome, botulism) or hypocalcemia (low calcium levels). The drug should be discontinued and mechanical respiratory assistance provided if needed if signs of respiratory paralysis occur during therapy.
GENTAMICIN-0.3%W/WOther disorders of ear, not elsewhere classified
Severe
How does the disease interact with Gentlee Cream 20 gm:
Aminoglycosides can harm the eighth cranial nerve, causing vestibular and/or auditory toxicity. Dizziness, nystagmus, vertigo, ataxia, tinnitus, and varied degrees of hearing impairment are among the symptoms. Following the discontinuation of the medicine, permanent hearing loss, including whole or partial irreversible bilateral deafness, may occur. Therapy with aminoglycosides, especially if extended (> 10 days), should be used with caution in patients with preexisting vestibular and/or auditory impairment, as it may delay or obfuscate the diagnosis of a drug-induced ototoxic impact. Patients should be adequately hydrated, the usual aminoglycoside dosage should not be exceeded, use with other ototoxic agents should be avoided, and peak and trough serum aminoglycoside concentrations should be determined on a regular basis and dosage adjusted to maintain desired levels.
How to manage the interaction:
Therapy should be administered with caution in patients with ototoxicity. The dosage should be reduced or therapy shoule be withdrawn if signs and symptoms of toxicity develop.
Aminoglycosides can harm the eighth cranial nerve, causing vestibular and/or auditory toxicity. Dizziness, nystagmus, vertigo, ataxia, tinnitus, and varied degrees of hearing impairment are among the symptoms. Following the discontinuation of the medicine, permanent hearing loss, including whole or partial irreversible bilateral deafness, may occur. Therapy with aminoglycosides, especially if extended (> 10 days), should be used with caution in patients with preexisting vestibular and/or auditory impairment, as it may delay or obfuscate the diagnosis of a drug-induced ototoxic impact. Patients should be adequately hydrated, the usual aminoglycoside dosage should not be exceeded, use with other ototoxic agents should be avoided, and peak and trough serum aminoglycoside concentrations should be determined on a regular basis and dosage adjusted to maintain desired levels.
How to manage the interaction:
Therapy should be administered with caution in patients with ototoxicity. The dosage should be reduced or therapy shoule be withdrawn if signs and symptoms of toxicity develop.
GENTAMICIN-0.3%W/WUnspecified kidney failure
Severe
How does the disease interact with Gentlee Cream 20 gm:
Aminoglycosides have the potential to be ototoxic and nephrotoxic. Damage to the eighth cranial nerve can cause vestibular and/or auditory toxicities such as dizziness, nystagmus, vertigo, ataxia, tinnitus, and varied degrees of hearing impairment. Tubular necrosis, increases in BUN, nonprotein nitrogen, and serum creatinine concentration, decreases in urine specific gravity and creatinine clearance, proteinuria, and cells or casts in the urine are all signs of nephrotoxicity. Rarely, renal electrolyte wasting can cause hypocalcemia, hypomagnesemia, and hypokalemia, which can be accompanied with paresthesia, tetany, disorientation, and positive Chvostek and Trousseau symptoms. Although aminoglycoside-induced nephrotoxicity is often reversible after treatment withdrawal, mortality from uremia has happened on rare occasions. Patients with renal impairment should be treated with caution and at lower doses of aminoglycosides, as they may be at risk.Drug buildup increases the risk of oto- and nephrotoxicity. Patients should be adequately hydrated, the usual aminoglycoside dosage should not be exceeded, use with other neuro- and nephrotoxic agents should be avoided, and peak and trough serum aminoglycoside concentrations should be determined on a regular basis and dosage adjusted to maintain desired levels. If toxicity develops, renal and eighth cranial nerve function should be constantly monitored, and the dosage lowered or therapy discontinued.
How to manage the interaction:
Therapy should be administered cautiously at reduced dosages in patients with kidney impairment. Patients should be adequately hydrated, the dose should not be exceeded, and use with other neuro- and nephrotoxic agents should be avoided to minimize the risk of toxicity.
Aminoglycosides have the potential to be ototoxic and nephrotoxic. Damage to the eighth cranial nerve can cause vestibular and/or auditory toxicities such as dizziness, nystagmus, vertigo, ataxia, tinnitus, and varied degrees of hearing impairment. Tubular necrosis, increases in BUN, nonprotein nitrogen, and serum creatinine concentration, decreases in urine specific gravity and creatinine clearance, proteinuria, and cells or casts in the urine are all signs of nephrotoxicity. Rarely, renal electrolyte wasting can cause hypocalcemia, hypomagnesemia, and hypokalemia, which can be accompanied with paresthesia, tetany, disorientation, and positive Chvostek and Trousseau symptoms. Although aminoglycoside-induced nephrotoxicity is often reversible after treatment withdrawal, mortality from uremia has happened on rare occasions. Patients with renal impairment should be treated with caution and at lower doses of aminoglycosides, as they may be at risk.Drug buildup increases the risk of oto- and nephrotoxicity. Patients should be adequately hydrated, the usual aminoglycoside dosage should not be exceeded, use with other neuro- and nephrotoxic agents should be avoided, and peak and trough serum aminoglycoside concentrations should be determined on a regular basis and dosage adjusted to maintain desired levels. If toxicity develops, renal and eighth cranial nerve function should be constantly monitored, and the dosage lowered or therapy discontinued.
How to manage the interaction:
Therapy should be administered cautiously at reduced dosages in patients with kidney impairment. Patients should be adequately hydrated, the dose should not be exceeded, and use with other neuro- and nephrotoxic agents should be avoided to minimize the risk of toxicity.
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