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نتيجة التلخيص (50%)

Metabolism and Excretion The metabolic fate of a particular agent largely depends on the chemical linkage between the aromatic residue and the rest of the molecule.Alternatively, severe hepatic disease or reduced hepatic blood flow may produce systemic intolerance to lidocaine and presumably other local anesthetics dependent on adequate liver function for their metabolism.The rapid bio- transformation of articaine to articainic acid (an essentially inactive metabolite) coupled with an unusually extensive tissue distribution significantly reduces the potential for cumulative toxicity after repeat dosing.78 Some local anesthetic metabolites retain significant phar- macologic activity and may contribute to drug toxicity.The initial reaction is usually N-dealkylation of the tertiary amino terminus, principally by CYP3A4 and CYP1A2.64,89 The resultant secondary amine of most amides is susceptible to hydrolysis by hepatic amidase activity, but conjugation, hydroxylation, and further dealkylation may also occur.Much of the sedative effect of lidocaine has been attributed to its de-ethylated metabolites monoethylglycinexylidide and gly- cinexylidide.82 As with the ester compounds, minimal amounts (1% to 20%) of administered amides appear in the urine as unmetabolized compounds.Hepatic blood flow seems to be the rate-limiting factor gov- erning metabolism of lidocaine and some other amides; elimi- nation half-lives range from 1.5 to 3.5 hours.


النص الأصلي

Metabolism and Excretion
The metabolic fate of a particular agent largely depends on the chemical linkage between the aromatic residue and the rest of the molecule. Ester drugs are inactivated by hydrolysis. Derivatives of p-aminobenzoic acid (e.g., procaine and tetracaine) are preferentially metabolized in the plasma by pseudocholinesterase; the ratio between plasma and tissue hydrolysis with other esters is variable. Products of hydrolytic cleavage may undergo further biotransformation in the liver before being eliminated in the urine. The half-life for the hydrolysis of procaine is normally less than 1 minute and less than 2% of the drug is excreted unchanged by the kidneys.
Metabolism of amide drugs primarily occurs in the liver. The initial reaction is usually N-dealkylation of the tertiary amino terminus, principally by CYP3A4 and CYP1A2.64,89 The resultant secondary amine of most amides is susceptible to hydrolysis by hepatic amidase activity, but conjugation, hydroxylation, and further dealkylation may also occur. Hepatic blood flow seems to be the rate-limiting factor gov- erning metabolism of lidocaine and some other amides; elimi- nation half-lives range from 1.5 to 3.5 hours. Inactivation of prilocaine, a secondary amine, is unusual because dealkylation is not required before hydrolysis can take occur, which may explain why almost half of its metabolism is extrahepatic. Articaine is also atypical because it is inactivated in the blood and other tissues by hydrolysis of an ester side chain required for local anesthetic activity. With an initial plasma half-life of approximately 25 minutes, articaine is removed from the circulation faster than other injected amides. The rapid bio- transformation of articaine to articainic acid (an essentially inactive metabolite) coupled with an unusually extensive tissue distribution significantly reduces the potential for cumulative toxicity after repeat dosing.78
Some local anesthetic metabolites retain significant phar- macologic activity and may contribute to drug toxicity. Much of the sedative effect of lidocaine has been attributed to its de-ethylated metabolites monoethylglycinexylidide and gly- cinexylidide.82 As with the ester compounds, minimal amounts (1% to 20%) of administered amides appear in the urine as unmetabolized compounds.
Differences in biotransformation of the various local anes- thetics are sometimes clinically relevant. Individuals with certain genetically based defects in pseudocholinesterase activity are unusually sensitive to procaine and other esters (but presumably not articaine); conventional doses of these drugs may occasionally lead to toxic reactions. Alternatively, severe hepatic disease or reduced hepatic blood flow may produce systemic intolerance to lidocaine and presumably other local anesthetics dependent on adequate liver function for their metabolism.


تلخيص النصوص العربية والإنجليزية أونلاين

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