Med Review Paralytics Flashcards

1
Q

What is the MOA of succinylcholine?

A

2 molecules of ACh bound together that mimic ACh and bind to ACh receptors at the NMJ ⇒ opens the channel and prevents resetting of the channel ⇒ paralysis

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2
Q

How is succinylcholine metabolized?

A

plasma cholinesterase

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3
Q

What major considerations must be made with administration of succinylcholine?

A
  • MH trigger
  • avoid in burn pt (upregulation of nACh receptors)
  • avoid in renal failure (further increase in K⁺)
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4
Q

Cisatracurium is how much more potent and atracurium?

A

4 times more potent than atracurium

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5
Q

Why would cisatracurium be the drug of choice for a patient with renal failure?

A

metabolized via hoffman elimination, organ independent

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6
Q

How is vecuronium metabolized?

A

hepatic metabolism (30-40%)

  • may accumulate in renal failure
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7
Q

How is rocuronium metabolized?

A

minimal to no metabolism

  • excreted unchanged in urine and bile
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8
Q

What considerations should be made with administration of rocuronium with liver failure? Renal failure?

A
  • Moderate prolongation in liver failure
  • not affected by renal failure
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9
Q

How is rocuronium administration affected in elderly and pregnant patients?

A

slightly prolonged in both

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10
Q

What is the most common acetylcholinesterase inhibitor used to reverse paralytics?

A

Neostigmine (prostigmin)

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11
Q

What is the onset of action for edrophonium in paralytic reversal?

A

1-2 minutes

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12
Q

What is the onset for pyridostigmine in paralytic reversal?

A

16 minutes

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13
Q

What is the onset for neostigmine in paralytic reversal?

A

~5 - 10 minutes

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14
Q

What is the duration of action for edrophonium in paralytic reversal?

A

5-20 minutes

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15
Q

What is the duration of action for neostigmine in paralytic reversal?

A

40 - 60 minutes

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16
Q

what is the duration of action for pyridostigmine in paralytic reversal?

A

90 minutes

17
Q

What drug is typically administered with acetylcholinesterase inhibitors to prevent profound bradycardia?

A

glycopyrrolate (robinul)

18
Q

What is the onset and duration of glycopyrrolate?

A

Onset: 2-3 minutes
Duration: 2 hours

19
Q

How does glycopyrrolate differ from administration of atropine?

A
  • does not cross the BBB and thus doesn’t cause sedation
  • also causes less tachycardia than atropine
20
Q

What are the main effects of glycopyrrolate?

A
  • tachycardia
  • bronchodilation
  • anti-sialogogue
21
Q

Sugammadex (bridion) works best in reversal of which paralytic?

A

FDA approved for Rocuronium reversal

has also been shown to work with vecuronium and pancuronium

22
Q

A shallow/medium blockade reversal can be done with what dose of sugammadex?

A

2 mg/kg

23
Q

A deep blockade reversal can be done with what dose of sugammadex?

A

4 mg/kg

24
Q

For immediate reversal, 3 minutes after administration of max 1.2mg/kg rocuronium what dose of sugammadex can be given for reversal?

A

16 mg/kg?