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Apex > Unit 5 Pharmacology: Neuromuscular Blocker Reversal Agents > Flashcards

Unit 5 Pharmacology: Neuromuscular Blocker Reversal Agents Flashcards

1
Q

What type of bond is formed when edrophonium binds to the anionic site on acetylcholine?

A

Electrostatic

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2
Q

Acetylcholinesterase hydrolyzes Ach into what 2 things?

A

Choline and acetate

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3
Q

How to drugs such as edrophonium, neostigmine, and pyridostigmine work?

A

They reversibly inhibit acetylcholinesterase which indirectly increases the concentration of acetylcholine at the neuromuscular junction, since more Ach is present it is better able to compete for alpha binding sites on the nicotinic receptor and antagonize the block. The NMB must still be eliminated from the body!

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4
Q

Pseudocholinesterase is inhibited by what NMB reversal agents? What does this mean?

A

neostigmine and pyridostigmine.

If sux is given after one of these reversal agents, duration of sux will be prolonged

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5
Q

What are the 2 ways AchE inhibitors increase the concentration of Ach at the nicotinic receptor?

A

Enzyme inhibition

Presynaptic effects

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6
Q

What are the 3 ways to inhibit AchE? What type of inhibition is each one? What drug(s) do this?

A
  1. Electrostatic attachment
    Competitive inhibition
    Edrophonium
  2. Formation of carbamyl esters
    Competitive inhibition
    Neostigmine, pyridostigmine, physostigmine
  3. Phosphorylation
    Non-competitive inhibition
    Organophosphates and echothiophate
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7
Q

What are the 2 possible mechanisms that AchE inhibitors have presynaptic site of action?

A
  1. Similar to sux, AchE inhibitors stimulate the presynaptic receptor and cause it to release additional Ach
  2. Inhibition of AchE near the presynaptic receptor increases the concentration of Ach in this region, so it is actually Ach that stimulates this receptor
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8
Q

What is the primary mechanism of edrophonium most likely?

A

Presynaptic

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9
Q 
Edrophonium:
Dose
Onset
Duration
Metabolism & Elimination
Best pairing
A 
Dose: 0.5 - 1.0 mg/kg
Onset: 1 -2 min
Duration: 30 - 60 min
Metabolism & Elimination: Renal 75%, liver 25%
Best pairing: atropine
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10
Q 
Neostigmine:
Dose
Onset
Duration
Metabolism & Elimination
Best pairing
A 
Dose: 0.02 - 0.07 mg/kg
Onset: 5 - 15 min 
Duration: 45 - 90 min
Metabolism & Elimination: Renal 50%, liver 50%
Best pairing: Glycopyrrolate
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11
Q 
Pyridostigmine:
Dose
Onset
Duration
Metabolism & Elimination
Best pairing
A 
Dose: 0.1 - 0.3 mg/kg
Onset: 10 - 20 min
Duration: 60 - 120 min
Metabolism & Elimination: Renal 75%, liver 25%
Best pairing: Glycopyrrolate
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12
Q

What is the significance of renal failure with reversing NMBs?

A

Renal failure prolongs both duration of action for both AchE inhibitors and NMBs, so there is no need to adjust dose or re-dose.

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13
Q

AchE inhibitors have a ceiling effect? T/F

A

True

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14
Q

The onset of action of AchE inhibitors is directly related to what?

A

Depth of block

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15
Q

Mixing AchE inhibitors yields what type of effect?

A

Additive

1 + 1 = 2

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16
Q

When compared to adults, antagonism with neostigmine is (faster or slower) in infants and children

A

Faster

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17
Q

Which AchE inhibitors do not cross the BBB? Why?

A

Edrophonium, neostigmine, and pyridostigmine

They are quaternary amines

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18
Q

What AchE inhibitor does cross the BBB? Why?

A

Physostigmine

It is a tertiary amine

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19
Q

Besides reversal of NMB, what other use does neostigmine have in the OR? How about physostigmine?

A

Neostigmine: intrathecal (50- 100mcg) produces analgesia. Side effects include N/V, pruritus, and prolongation of sensory and motor block
Physostigmine: 40mcg/kg reduces the incidence of post op shivering. Its efficacy matches meperidine and clonidine.

20
Q

By increasing the concentration of Ach at the muscarinic receptor, AchE inhibitors cause a predictable set of ________

A

Parasympathetic side effects

Cholinergic side effects

21
Q

Mnemonic for cholinergic side effects:

A 
Diarrhea
Urination
Miosis 
Bradycardia
Bronchoconstriction
Emesis
Lacrimation
Laxation
Salivation
22
Q

What muscarinic antagonist (anticholinergic) increases HR the most?

A

Atropine

23
Q

What muscarinic antagonist (anticholinergic) produces the most sedation?

A

Scopolamine

24
Q

What muscarinic antagonist (anticholinergic) does not cause sedation?

A

Glycopyrrolate

25
Q

What muscarinic antagonist (anticholinergic) is the best antisialagogue?

A

Scopolamine

26
Q

What muscarinic antagonist (anticholinergic) produces the most mydriasis?

A

Scopolamine

27
Q

What muscarinic antagonist (anticholinergic) prevents motion induced nausea the best?

A

Scopolamine

28
Q

What muscarinic antagonist (anticholinergic) decreases gastric H+ secretion the most?

A

All about equal

29
Q

What muscarinic antagonist (anticholinergic) produces no mydriasis?

A

Glycopyrrolate

30
Q

What muscarinic antagonist (anticholinergic) does not prevent motion induced nausea?

A

Glycopyrrolate

31
Q

What muscarinic antagonist (anticholinergic) produces the best smooth muscle relaxation?

A

Equal between atropine and Glycopyrrolate

32
Q

Atropine and scopolamine are naturally occurring ______, what does this mean?

A

Tertiary amines.

They are lipophilic and cross the BBB, GI tract, and placenta

33
Q

Why can’t Glycopyrrolate cross lipid barriers?

A

It is a quaternary ammonium derivative, it is ionized. So it does not possess CNS activity or cross the placenta

34
Q

Small does of atropine have what paradoxical effect? Why?

A

Paradoxical bradycardia.
Probably due to inhibition of the presynaptic M1 receptor on vagal nerve endings whose job is to reduce Ach release via a negative feedback loop, if it’s blocked this turn off the loop and allows for continued Ach release and bradycardia

35
Q

Do muscarinic antagonist (anticholinergic) affect HR in transplant patients?

A

No. But they will experience the other cholinergic effects from AchE inhibitors and should still be given a muscarinic antagonist.

36
Q

What NMB does Sugammadex reverse?

A

The aminosteroids:

Roc > VEC > pancuronium

37
Q

What is the MOA of sugammadex?

A

A gamma-cyclodextrin made of 8 sugars assembled in a ring, the ring encapsulates the NMB rendering it inactive.

38
Q

What are the side effects of sugammadex?

A

Because it does not interact with neuromuscular receptors and neurotransmitters, it has no major systemic side effects

39
Q

How is the dose of sugammadex calculated? Why?

A

On the degree of block present, because there is a need for a 1:1 molar ratio between sugammadex and NMB

40
Q

Sugammadex dosing for Rocuronium:

A

TOF 2/4 or better 2 mg/kg
TOF 0/4 + 2 PTC or better 4 mg/kg
3 minutes after Roc 1.2 mg/kg or less - 16 mg/kg

41
Q

Sugammadex dosing with Vecuronium

A

TOF 2/4 or better 2 mg/kg

TOF 0/4 + 2 PTC or better 4 mg/kg

42
Q

How is sugammadex metabolized?

A

Sugammadex and the sugammadex-rocuronium complex are excreted unchanged by the kidneys

43
Q

What can you do if a patient needs to be paralyzed after receiving Sugammadex?

A

Use a benzylisoquinolinium or Succinylcholine - If 16 mg/kg of sugammadex was used, only option.
If 4 mg/kg or less was used you can redoes roc or vec:
If between 5 min to 4 hours - roc 1/2 mg/kg
If more than 4 hours roc 0.6 mg/kg or vec 0.1 mg/kg

44
Q

How common is anaphylaxis with sugammadex?

A

0.3% of patients

45
Q

What complications have been reported with sugammadex?

A

Bradycardia

Cardiac arrest

46
Q

What may be of particular concern with sugammadex use in adult females?

A

It binds oral contraceptives

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