neuromuscular blockers Flashcards

1
Q

Inside of cell is negative or positive at rest? When depolarized?

A

At rest= negative, depolarized= positive

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2
Q

what type of neurons are motor neurons? where do they orginate?

A

alpha motor neurons, from anterior horn of spinal cord

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3
Q

steps of AP to ACh channels opening

A
  1. AP moves along motor neuron (Nn) towards muscle fiber
  2. AP voltage opens Ca Channels (allows for ACH vesicles to move to presynpatic terminal)
  3. ACh is released at motor end plate
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4
Q

steps after ACh release

A
  1. some ACh binds to prejunctional receptors on Nn (these mobilize ACh vesicles to move from stockpile to front line)
  2. ACh molecules bind to acetoylchoine receptors on NMJ motor endplate
  3. 2 ACh molecules attach to 2 alpha subunits on AChreceptor, allowing Na in
  4. positive potential coming in opens up voltage gated Na channels, depolarizes muscle membrane
  5. causes SR to release large amounts of Ca ions
  6. Ca ions intiate attraction between actin and myosin for contraction
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5
Q

what are the 2 types of AChreceptors

A
  1. fetal (lower conductance cation channel with longer opening times - more K release)
  2. adult
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6
Q

how does muscle contraction terminate

A

Ach diffuses away or gets removed by acetylcholinesterase

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7
Q

types of NMBs

A
  1. depolarizing (agonists)
  2. non depolarizing (competitive antagonists)
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8
Q

what are the different type of NDNMBs

A

steriods or benzylquinolones

short acting, intermediate acting, long acting

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9
Q

MOA of Sch

A

densensitization of Nm receptor

sustained depolarization does not allow for Nm to reset (hyperpolarization)

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10
Q

metabolism of SCh

A

hydrolyzed by butrylcholinesterase (plasma cholinesterae) … synthesized in liver

needs to diffuse out of NMJ to terminate action

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11
Q

dose of SCh

A

1-1.5 mg/kg

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12
Q

onset of Sch

A

30- 60 seconds

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13
Q

duration of Sch

A

5-10 minutes

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14
Q

side effects of SCh

A

Fasiculations (Sch only needs to bind to 1 alpha receptor, can bounce from channel to channel, thus they stay open longer), histamine release, cardiac muscarinc binding (SB, JR, Sinus arrest), hyperK, increased intraocular/intragastric/intracrainial pressure, myogolbinura, massesseter spasm

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15
Q

What type of pts have issues with breaking down SCh

A

-decreased hepatic function
-drug-induced decreases (neo, reglan, chemo)
-chronic diseases
-pregnancy
-obesity (increased activity of plasma cholinesterase)

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16
Q

how can you help treat fasciculations?

A

pre-dose with small dose NDMR

17
Q

disease that causes resistance to SCh

A

MG (less Nm receptors, need more SCh - like 2.0mg/kg)

18
Q

Which NDMR are steriods and which are quinolones?

A

Steriods= PVR

pancuronium
vecuronimum
rocuronium

Benzylquinolones= atracurium and cisatracurium

19
Q

difference between steriod and quinolones?

A

steroids= eliminated by hepatic mostly (pan= renal)

quinolones= hoffman elimination (cis) or plasma cholinesterase (miv) (spontaneous breakdown at certain pH and temperature)

20
Q

which drugs release histamine?

A

SAM

Sch, atracurium, morphine

21
Q

adverse side effects of NDMRs

A

Cardiac - effects at cardiac muscariac receptors and autonomic ganglia

pancuronium- blocks vagal response (increases HR & CO, no change in SVR)

22
Q

conditions that prolong NDMRs

A

VA, antibiotics (aminoglycosides, tetracyclines and clindaymacin), hypocalcemia, hypermagnesemia, LAs, hypothermia, dantrolene

23
Q

intubating doses for NDMRs

A

all are mg/kg

Mivacurium (0.2-0.25)

Rocuronium (0.6-1.2)

Vecuronium (0.1-0.2)

Atracurium (0.5-0.6)

Cisatracrium (0.15-0.2)

Pancuronium (0.08-0.12)

24
Q

onset of NDMRs

A

In minutes

Mivacurium (2-3)

Rocuronium (1-3) *

Vecuronium (2-3)

Atracurium (1-3)

Cisatracrium (2-3)

Pancuronium (3-5)

  • when Roc given at 1.2 mg/kg onset is the same as Sch, with longer duration
25
Q

DOA of NDMRs & Sch

A

In minutes

SCh (6-11)

Mivacurium (15-20)

Rocuronium (50-60)

Vecuronium (40-60)

Atracurium (40-60)

Cisatracrium (40-60)

Pancuronium (90)

26
Q

what are alternatives is NMBAs are contraindicated?

A

High dose opioid on induction (I.e. remi 4-5 mcg/kg with propofol)

**should give glycopyrollate at same time (0.2-0.4 mg IV) due to brady

27
Q

which nondepolarizing NMBA most commonly causes anaphylaxis d/t histamine release? which one most commonly causes anaphylactoid rxn (nonIgE histamine release)?

A
  1. roc
  2. ata

***Note: drugs with single quaternary ammonium group are less likely to cause anaphylaxis than SCh, but cross sensitivity can occur.
*SCh is most common NMB to have anaphylaxis to

28
Q

what is the mechanism of fade for NDMR vs SCh?

A

NDMR: Nn ACh receptors are blocked (stops signal to move stockpile SCh to front line.. less ACh available to use after multiple depolarizations) (phase II block)

Sch: stimulates Nn receptors same as ACh… stimulates ACh release repeatedly (phase I block) *

  • high dose SCh causes phase II block
29
Q

explain mechanism of TOF

A

delivers 4 successive electric stimuli at a frequency of 2 Hz (2 stimulations per second)

if all 4 twitches present= ratio 1

adequate recovery = 0.9

30
Q

Other names for Cisatricurium, vecuronium, Rocuronium, pancuronium, Sch

A

Cis-Nimbex
Vec-Nornuron
Pan- pavulon
Roc-Zemuron
Sch- Anectine

31
Q

disapperance of twitches happens at what % receptor capactiy

A
  • 4th twitch disappears at 75-80% occupancy
  • 3rd twitch disappears at 85% occupancy
  • 2nd twitch disappears at 85-90% occupancy
  • 1st twitch disappears at 90-95% occupancy
32
Q

explain mechanism of tetantic stimulation

A

continuous, high frequeuncy 50 or 100 Hz (50 or 100 stimulations per second) causes sustained muscle contraction

33
Q

explain the sequence of blockade

A

central muscles blocked before and recover faster than peripheral

34
Q

best place to measure onset of blockade (intubation conditions)

A

muscle= orbicularis oculi or corrugator supercilli

nerve= facial nerve

35
Q

best place to measure recovery

A

muscle= adductor pollicis
nerve= ulnar nerve