Unit 5 - NMB Reversals & Anticholinergics Flashcards

1
Q

what metabolizes succs

A

pseudocholinesterase

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2
Q

acetylcholinesterase inhibitors that antagonize pseudocholinesterase

A

neostigmine & pyridostigmine (not edrophonium)

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3
Q

where is AChE concentrated

A

around nicotinic receptors at NMJ

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4
Q

acetylcholinesterase inhibitors that inhibit AChE

A

Edrophonium, neostigmine, and pyridostigmine

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5
Q

how do acetylcholinesterase inhibitors antagonize block with NDNMB

A

inc. concentration of ACh at NMJ

more ACh available to antagonize the block

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6
Q

2 ways AChE inhibitors increase ACh at nicotinic receptor

A

1) enzyme inhibition, 2) presynaptic effects

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7
Q

Primary mechanism of edrophonium

A

most likely presynaptic

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8
Q

MOA of edrophonium

A
  • forms electrostatic bond at anionic site and a noncovalent H+ bond at the esteratic site (short duration of action, H+ bonds are weak)
  • competitive
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9
Q

2 possible mechanisms of presynaptic action:

A
  1. Similar to succs, AChE inhibitors stimulate presynaptic receptor = additional ACh release
  2. Inhibition of AChE near presynaptic receptor increases ACh concentration in that region
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10
Q

is a dose adjustment of AChE inhibitors needed for renal failure

A

nope - duration of NMBs also prolonged

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11
Q

effect of mixing AChE inhibitors

A

additive effect

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12
Q

neostigmine antagonism is faster in children or adults?

A

infants & children

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13
Q

which AChE inhibitor(s) pass the BBB

A

only Physostigmine (tertiary amine)

Edrophonium, neostigmine, & pyridostigmine are quaternary amines (do not

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14
Q

risks of extubating with TOF ratio < 0.9

A

↑ risk airway obstruction, hypoxemic events, postop pulm. complications

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15
Q

effect of giving AChE inhibitor at full recovery

A

paradoxical muscle weakness

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16
Q

dose of intrathecal neostigmine that produces analgesia

A

50-100 mcg

17
Q

SEs of intrathecal neostigmine

A
  • N/V
  • pruritis
  • prolonged sensory and motor block
18
Q

AChE inhibitor that can be used for postop shivering

A

Physostigmine (40 mcg/kg)

19
Q

4 drugs that ↓ shiving in PACU:

A

physostigmine, meperidine, clonidine, dexmedetomidine

20
Q

cholinergic side effects

r/t ↑ concentration of ACh at muscarinic receptor

A

DUMBBELLS
* Diarrhea
* Urination
* Miosis
* Bradycardia
* Bronchoconstriction
* Emesis
* Lacrimation
* Laxation (elimination of fecal waste)
* Salivation

21
Q

how do antimuscarinics affect HR

A

increase
atropine > glyco > scopolamine

22
Q

most to least antisialogogue effects of anticholinergics

A

scopolamine > glycopyrollate > atropine

23
Q

how do anticholinergics affect gastric H+ secretion

A

increased

24
Q

Job of M1 receptor

A
  • to reduce ACh release via negative feedback loop
  • blockade “turns off” loop and allows continued ACh release/bradycardia
25
Q

can anticholinergics be given to a patient with a transplanted heart

A
  • Do not affect HR in patients with previous heart transplant (denerevated heart)
  • Can still experience other cholinergic effects from AChE inhibitors - give with AChE inhibitors
26
Q

MOA of sugammadex

A
  • gamma-cyclodextrin made of 8 sugars assembled in a ring
  • ring encapsulates the NMB & renders it inactive/unable to engage with nicotinic receptor
  • Encapsulating ↓ free concentration of drug in plasma  augments concentration gradient between NMJ & plasma
27
Q

which NMBs does sugammadex reverse

A

Roc > vec > pancuronium

28
Q

excretion of sugammadex

A

Excreted unchanged by kidneys

29
Q

sugammadex dose after roc with TOF 2/4 or better

A

2 mg/kg

30
Q

sugammadex dose after roc with TOF 0/4 + 1 PTC or better or better

A

4 mg/kg

31
Q

what NMB should be used if pt needs to be paralyzed after 16 mg/kg sugammadex

A

Use NMB from outside aminosteroid class (succs, atracurium, cisatracurium…) for 24 hours

32
Q

re-dosing roc after reversed with < 4 mg/kg sugammadex

A
  • Can give 1.2 mg/kg roc if relaxant needed between 5 min-4 hours of admin.
  • > 4 hours, can give roc at 0.6 mg/kg or vec 0.1 mg/kg
33
Q

AEs of sugammadex

A
  • anaphylaxis
  • bradycardia
  • reduces effectiveness of hormonal contraceptives for up to 7 days
34
Q

neostigmine MOA

A

reversibly binds to AChE at NMJ by forming a carbamyl ester complex at esteratic site, competitively antagonizes acetylcholine hydrolysis

35
Q

why is physostigmine the only AChE inhibitor used to treat anticholinergic crisis

A

only AChE inhibitor that crosses BBB

15-60 mcg/kg

36
Q

s/s anticholinergic syndrome

A

confusion, agitation, hallucinations, somnolence, unconsciousness

Often mistaken as slow emergence from anesthesia

37
Q

job of M1 receptor on vagal nerve endings

A

to reduce ACh release via negative feedback loop

blockade “turns off” loop and allows continued ACh release/bradycardia

explains why small doses of atropine can cause paradoxical bradycardia d/t inhibition of presynaptic M1 receptors on vagal nerve endings

38
Q

MOA of organophosphates

A

Produce non-reversible inhibition of AChE by forming a stable complex with esteratic site