TYK13 - Revision history

WikiSysop at 22:56, 22 January 2022

2022-01-22T22:56:09Z

← Older revision		Revision as of 22:56, 22 January 2022
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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>
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	==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]
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	==Keywords==		==Keywords==
	:

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WikiSysop: 1 revision imported

2021-03-05T02:34:29Z

1 revision imported

← Older revision	Revision as of 02:34, 5 March 2021
(No difference)

metawikimedia>JustinHamrick at 13:20, 14 February 2015

2015-02-14T13:20:30Z

New page

__NOTOC__
<div class="mw-collapsible mw-collapsed" style="width:100%">
All of the following medications are known to ENHANCE neuromuscular blockade EXCEPT:

A. Volatile agents

B. Local anesthetics

C. Aminoglycosides

D. Furosemide

E. Phenytoin

<div class="mw-collapsible-content">
==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==
<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]
</div>

==Keywords==
:

</div>
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<p style="text-align: center;">[[TYK About | About Test Your Knowledge]]</p>