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Anesthesia Pharm Exam 2 > NMDRs > Flashcards

NMDRs Flashcards

1
Q

NMJ Transmission Function

A
  • ACh synthesized and stored in synaptic veicles
  • AP stimulates distal motor nerve
  • Ca++ diffuses into terminal and VGCaCh open
  • synaptic vesicles fuse to membrane
  • ACh released into cleft
  • presynaptic nicotinic receptor responds to ACh by synthesizing more and mobilizing ACh vesicles (+ feedback)(phII block w Sux related to this)
  • ACh binds to nicotinic ACh receptors on surface of post-synaptic membrane
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2
Q

Cholinergic

A

releases ACh

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3
Q

Adrenergic

A

releases NE

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4
Q

Pre/Post Ganglionic NTs

A

PNS pre and post = ACh

SNS pre = ACh

SNS post = NE

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5
Q

ACh is hydrolized by ____ to ____ and _____

A

ACh is hydrolized by acetylcholinesterase (AChE) to acetate and choline

  • choline taken up by presynaptic terminal for resynthesis of ACh
  • acetate diffuses away
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6
Q

The release of NT is dependent on the entry of Ca++

A

HYPOcalcemia = decreases NT release (weakness)

HYPERcalcemia = increases NT release (tetany)

HYPOmagnesemia = increases NT release

HYPERmagenesemia = decreases NT release

- the actions of Ca++ and Mg+ are antagonistic at presynaptic nerve terminals

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7
Q

ACh receptors - A subunits

A

both A subunits must be occupied to get contraction! Block one = no contraction. Sux lands on both and we get depolarization

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8
Q

Up-regulated AChRs (denervation injuries - burns)

A

– AChr agonists see increased sensitivity

– AChr antagonists see decreased sensiCvity

• Nondepolarizing muscle relaxants (NDMR) are AChr antagonists

– These patients require increased dosages or shorter redosing intervals of the NMDRs

anesthesia on a burn patient requires frequent redoxing due to upregulation of receptors!

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9
Q

Down-regulated AChRs (myasthenia gravis)

A

– ACHr agonists see decreased sensitivity and require higher dosages

– ACHr antagonists see increased sensitivity and require lower dosages and longer intervals between redosing

our NMDRs are ANTagonists therefore we require higher AGonists

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10
Q

Depolarizing Muscle Relaxants (Sux)

A
  • depolarize the nACHr - NOT competitive
  • action similar to ACh (ACh depolarizes the NMJ and is rapidly metabolized by AChE)
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11
Q

Sux (depolarizing)

A
  • attaches to the 2 A subunits and depolarizes
  • metabolized by BCH-esterase (not present in the NMJ)
  • after depolarization, sux remains in the synaptic cleft until plasma level lowers and creates a concentration gradient out of the cleft
  • after moving out of the cleft, circulating BCH-esterase metabolizes the remaining sux.
  • 80-90% of the sux is metabolized in the blood on the way to the NMJ! (so only 10-20% of the dose is giving us action)
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12
Q

NON-depolarizing muscle relaxants

A
  • competitive: compete for ACh binding sites on nicotinic receptor
  • when bound, it prevents ion channel from opening
  • NDMRs completely BLOCK ACh from binding to receptor… post-synaptic membrane remains polarized
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13
Q

Non-Depolarized Block

A
  • is from competitive inhibition of nAChR
  • shows fade on TOF monitor
  • can see post-tetanic facilitation (increase in TOF after tetanic stimulation)
  • can be antagonized (reversed) by anticholinesterases
  • do NOT see fasiculations (no depolarization)
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14
Q

Succinylcholine

A

DOA: ultrashort

Onset: 0.5-1.5 min

Duration to 25% recovery: 6-8 min

ED95: 0.25 - 0.30

SE: histamine release, tachycardia (brady in peds), decresed BP

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15
Q

Atracurium

A

DOA: Intermediate

Onset: 3-4 min

Duration to 25% recovery: 35-45 min

ED95: 0.15 - 0.25

SE: dose-dependent histamine release, small reflex tachycardia, minimal BP effect

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16
Q

Cisatracurium

A

DOA: Intermediate

Onset: 5-7 min

Duration to 25% recovery: 35-45 min

ED95: 0.05

SE: no effect on HR, BP, no histamine release

17
Q

Vecuronium

A

DOA: Intermediate

Onset: 3-4 min

Duration to 25% recovery: 35-45 min

ED95: 0.05

SE: no histamine release, minimal BP and HR effect

18
Q

Rocuronium

A

DOA: Intermediate

Onset: 1-1.5 min

Duration to 25% recovery: 30-40 min

ED95: 0.30

SE: no histamine release, minimal tachy in kids, minimal BP effect

19
Q

Mivacurium

A

DOA: Short

Onset: 3-4 min

Duration to 25% recovery: 15-20 min

ED95: 0.08

SE: dose-dependent histamine releae, minimal HR and BP effect

20
Q

What is the purpose of giving muscle relaxants?

A
  • to relax the skeletal muscles… more importantly to relax the VOCAL CORDS to pass the ETT through
21
Q

What are the benefits of muscle relaxation?

A
  • improve surgical conditions (CV, neuro, transplant surgeries)
  • facilitate endotracheal intubation
22
Q

What are the risks associated with muscle relaxation?

A
  • no analgesia
  • no anesthesia
  • paralyzed but not anesthetized = bad!
23
Q

ED50 of muscle relaxant

A

dose at which a muscle relaxant produces a 50% depression of twitch tension in the nACHr

24
Q

A depolarizing NMB (sux) does 3 things:

A
  1. desensitizes the nACHr
  2. inactivates the VGaNa Channel and the NMJ
  3. increases K+ permeability in the surrounding membrane
    * due to these effects, no AP can be generated and AChR blockade occurs!*
25
Q

Percentages of Twitch Response

A
  • twitch response may not be reduced until 70% of nAChR are blocked
  • twitch is completely elminated when 90% of receptors are blocked
26
Q

Peripheral Nerve Stimulation can answer 3 Questions:

A
  • is NMB adequate?
  • is it inadequate?
  • can it be antagonized?
  • you must know how to use TOF IOT answer these questions!*
27
Q

Clinical tests to monitor cessation of NMB

A
  • 5 second head lift
  • leg lift off OR table
  • strong handgrip from which you cannot remove 2 fingers
  • TV (only requires return of diaphragmatic tone) can pull 5mL/kg with 80% nAChR still occupied by NMDR
28
Q

Dibucaine Test

A

atypical BCE genetic variant, the dibucaine number communicates how inhibited the action of BCE is by dibucaine.

  • higher the number the more normal they are
  • low dibucaine number = longer DOA for sux
    ie: dibucaine number of 20-30 will prolong action of Sux up to 4-8 hours
29
Q

Treatment of Sux-induced Hyperkalemia

A
  1. hyperventilation (make them alkalotic)
  2. 1-2 mg Ca+ Chloride IV (helps w muscle contraction)
  3. 50cc D50W + 10 U IV Insulin (adults) or

1 ml/kg D50W + 0.15 U/kg insulin (peds)

  1. Na+ Bicarb 1 mEq/kg
30
Q

Dantrolene

A

Txs MH

  • initial dose 2 mg/kg
  • repeat 2 mg/kg up to 10 mg/kg if required
  • clinical response of decreased temp, decrease ETCO2 will indicate enough dantrolene has been given
  • redosing in PACU may be necessary
31
Q

MH may occur: (3 things)

A
  1. after multiple unremarkable anesthetics (previous sux exposure)
  2. during maintenace phase or post op from anesthesia
  3. in pts w no prior fam hx of MH
32
Q

Phase II Block

A
  • excessively large doses, repeat doses of Sux, or Sux infusions can result in a phase II block. This acts more like a non-depolarizing blockade of the NMJ.
  • if fade on TOF w a non-depolarizing block, the Sux has gone into a Ph II block.

>20 min reverse

monitor/extubate at 0.9.

33
Q

Anticholinesterases

A

Neostigmine, pyridostigmine, etc.

  • given to reduce the activity of enzymes that break down ACh to IOT reverse the effects of non-depolarizing muscle relaxants
  • standard at end of anesthetic cases
34
Q

2 groups of non-depolarizing muscle relaxants:

A

benzylisoquinolinium and

aminosteroid

35
Q

benzylisoquinolinium

A

d-tubocurarine (not in US)

metocurine (60 min, not in US)

atracurium (60 min)

cis-atracurium (30-60 min)

doxacurium (60+, not in US)

36
Q

aminosteroid compounds

A

pancuronium (60 min)

vecuronium (20-50 min)

rocuronium (most common, 20-50 min)

pipercuronium (60+ min, rarely used)

37
Q

NDMRs are _____ ______ chemical compounds that are positively charged

A

NDMRs are quaternary ammonium chemical compounds that are positively charged

38
Q
A

Anesthesia Pharm Exam 2 (5 decks)

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