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Flashcards in NMB Agents Deck (12):
1

Succinylcholine - speed of action

Rapid on & offset

2

Succinylcholine metabolism?

metabolized by pseudocholinesterases, people with atypical plasma pseudocholinesterases have extended clinical effects

3

How does sux work?

Binds, depolarizes and non-competitively inhibits acetylcholine receptors at NMJ

4

Fascilations which which drug?

Sux

5

Side effect of sux?

Transient increase in plasma potassium level, related to number of ACh receptors at NMJ, those with increased receptors at NMJ are at higher risk for hyperkalemia (like those with spinal cord injury), burns, immobility, NM disorder such as MD, but can be given in patients with renal failure if they have normal K

6

Non-depolarizing NMBs

Competitive antagonists, rocuronium, mivacurium, pancuronium, cisatracurium

7

Fast onset NMB

Rocuronium

8

NMB that causes tachycardia by vagolysis

Pancuronium

9

How are most NMBs degraded?

Liver/kidney

10

Cisatracurium clearance?

Degrases spontaneously in plasma - good for liver or kidney failure

11

Reversal of non-depolarizing NMBs

Neostigmine or edrophonium (Achesterase inhibitors) If you increase concentration of acetylcholine in NMJ you can clinically reverse effects of NMB, patient must have at least one visible twitch, then give acetylcholinesterase inhibitor

12

Side effect of acetylcholinesterase inhibitor?

Bradycardia because of action at muscarinic resceptors as well, must give anticholinergic agent with reversal (i.e. atropine or glycopyrrolate) to prevent bradycardia