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Which of the following halogenated agents is NOT associated with fulminant autoimmune hepatitis? | Which of the following halogenated agents is NOT associated with fulminant autoimmune hepatitis? | ||
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E. Isoflurane | E. Isoflurane | ||
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==Answer== | ==Answer== | ||
The answer is B. The first large study on halothane-associated liver injury reported an incidence of 1:35,000 for fatal hepatic necrosis after halothane anesthesia. Patients are thought to be at higher risk after repeated exposures. This is in contrast to a MILD form of hepatocelluar injury than can occur in 20% of patients after halothane anesthesia. The mild form involves a transient elevation in liver enzymes (ALT) and slight alterations in cellular integrity by electron microscopy. The metabolism of halogenated agents causes tissue acetylation. Antibodies against these neo-antigens is thought to be the mechanism of the severe type of hepatic injury. The onset for the severe type occurs at 4-7 days and is usually present with jaundice and fever. Enflurane, isoflurane, halothane, and desflurane have been reported to trigger this fulminant type. As sevoflurane is metabolized by a distinctly different pathway than the agents with a methyl-ethyl structure, the autoimmune response is not known to occur. The MILD injury can still occur. | The answer is B. The first large study on halothane-associated liver injury reported an incidence of 1:35,000 for fatal hepatic necrosis after halothane anesthesia. Patients are thought to be at higher risk after repeated exposures. This is in contrast to a MILD form of hepatocelluar injury than can occur in 20% of patients after halothane anesthesia. The mild form involves a transient elevation in liver enzymes (ALT) and slight alterations in cellular integrity by electron microscopy. The metabolism of halogenated agents causes tissue acetylation. Antibodies against these neo-antigens is thought to be the mechanism of the severe type of hepatic injury. The onset for the severe type occurs at 4-7 days and is usually present with jaundice and fever. Enflurane, isoflurane, halothane, and desflurane have been reported to trigger this fulminant type. As sevoflurane is metabolized by a distinctly different pathway than the agents with a methyl-ethyl structure, the autoimmune response is not known to occur. The MILD injury can still occur. | ||
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Latest revision as of 22:51, 23 January 2022
Which of the following halogenated agents is NOT associated with fulminant autoimmune hepatitis?
A. Halothane
B. Sevoflurane
C. Desflurane
D. Enflurane
E. Isoflurane
Answer
The answer is B. The first large study on halothane-associated liver injury reported an incidence of 1:35,000 for fatal hepatic necrosis after halothane anesthesia. Patients are thought to be at higher risk after repeated exposures. This is in contrast to a MILD form of hepatocelluar injury than can occur in 20% of patients after halothane anesthesia. The mild form involves a transient elevation in liver enzymes (ALT) and slight alterations in cellular integrity by electron microscopy. The metabolism of halogenated agents causes tissue acetylation. Antibodies against these neo-antigens is thought to be the mechanism of the severe type of hepatic injury. The onset for the severe type occurs at 4-7 days and is usually present with jaundice and fever. Enflurane, isoflurane, halothane, and desflurane have been reported to trigger this fulminant type. As sevoflurane is metabolized by a distinctly different pathway than the agents with a methyl-ethyl structure, the autoimmune response is not known to occur. The MILD injury can still occur.
Notes