TYK52: Difference between revisions

no edit summary
m (1 revision imported)
No edit summary
 
Line 1: Line 1:
__NOTOC__
__NOTOC__
<div class="mw-collapsible mw-collapsed" style="width:100%">
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?


Line 12: Line 11:


E. Isoflurane
E. Isoflurane
 
<div class="mw-customtoggle-TYK_Answer" style="text-align: right; color:#0000ff">Click for Answer</div>
 
<div class="mw-collapsible mw-collapsed" id="mw-customcollapsible-TYK_Answer">
 
<div class="mw-collapsible-content">  
==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.
==Notes==
==Notes==
<references />
<references />


==Keywords==
==Keywords==
:


</div>
</div>
----
----
----
----