TYK13: Difference between revisions
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All of the following medications are known to ENHANCE neuromuscular blockade EXCEPT: | All of the following medications are known to ENHANCE neuromuscular blockade EXCEPT: | ||
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E. Phenytoin | E. Phenytoin | ||
<div class="mw-customtoggle-TYK_Answer" style="text-align: right; color:#0000ff">Click for Answer</div> | |||
<div class="mw-collapsible- | <div class="mw-collapsible mw-collapsed" id="mw-customcollapsible-TYK_Answer"> | ||
==Answer== | ==Answer== | ||
The answer is E. All of the following enhance blockade except Phenytoin. Phenytoin and carabamazepine ANTAGONIZE the blockade by increasing the clearance of NMBDs through up regulation of hepatic metabolism. Volatile agents enhance blockade in a dose dependent manner (just ask Yaster), although how this occurs is not known. Local anesthetics, given in low doses, augment the blockade by inhibiting propagation along the nerve, an inhibiting release of acetylcholine (ACh) into the synaptic cleft. Aminoglycosides augment blockade with aminosteroid, but not benzylisoquiolinium neuromuscular blocking drugs (NMBD). Furosemide, in low doses (1mg/kg) augments the blockade by inhibiting cAMP production, leading to decreased ACh output. Note the hypokalemia (from diuretics) hyperpolarizes the membranes, requiring more ACh-receptor binding to stimulate membrane depolarization; hence, less NMBD is required for blockade (e.g. enhanced blockade). | The answer is E. All of the following enhance blockade except Phenytoin. Phenytoin and carabamazepine ANTAGONIZE the blockade by increasing the clearance of NMBDs through up regulation of hepatic metabolism. Volatile agents enhance blockade in a dose dependent manner (just ask Yaster), although how this occurs is not known. Local anesthetics, given in low doses, augment the blockade by inhibiting propagation along the nerve, an inhibiting release of acetylcholine (ACh) into the synaptic cleft. Aminoglycosides augment blockade with aminosteroid, but not benzylisoquiolinium neuromuscular blocking drugs (NMBD). Furosemide, in low doses (1mg/kg) augments the blockade by inhibiting cAMP production, leading to decreased ACh output. Note the hypokalemia (from diuretics) hyperpolarizes the membranes, requiring more ACh-receptor binding to stimulate membrane depolarization; hence, less NMBD is required for blockade (e.g. enhanced blockade). | ||
==Notes== | ==Notes== | ||
<references /> | <references /> | ||
[http://web.squ.edu.om/med-Lib/MED_CD/E_CDs/anesthesia/site/content/v02/020433r00.HTM Pharmacology of Muscle Relaxants and Their Antagonists] | [http://web.squ.edu.om/med-Lib/MED_CD/E_CDs/anesthesia/site/content/v02/020433r00.HTM Pharmacology of Muscle Relaxants and Their Antagonists] | ||
==Keywords== | ==Keywords== | ||
</div> | </div> | ||
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Latest revision as of 22:56, 22 January 2022
All of the following medications are known to ENHANCE neuromuscular blockade EXCEPT:
A. Volatile agents
B. Local anesthetics
C. Aminoglycosides
D. Furosemide
E. Phenytoin
Answer
The answer is E. All of the following enhance blockade except Phenytoin. Phenytoin and carabamazepine ANTAGONIZE the blockade by increasing the clearance of NMBDs through up regulation of hepatic metabolism. Volatile agents enhance blockade in a dose dependent manner (just ask Yaster), although how this occurs is not known. Local anesthetics, given in low doses, augment the blockade by inhibiting propagation along the nerve, an inhibiting release of acetylcholine (ACh) into the synaptic cleft. Aminoglycosides augment blockade with aminosteroid, but not benzylisoquiolinium neuromuscular blocking drugs (NMBD). Furosemide, in low doses (1mg/kg) augments the blockade by inhibiting cAMP production, leading to decreased ACh output. Note the hypokalemia (from diuretics) hyperpolarizes the membranes, requiring more ACh-receptor binding to stimulate membrane depolarization; hence, less NMBD is required for blockade (e.g. enhanced blockade).
Notes
Pharmacology of Muscle Relaxants and Their Antagonists