Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

CNS I > NM Blocking agents > Flashcards

NM Blocking agents Flashcards

1. Describe the neuromuscular junction, the motor endplate, nicotinic acetylcholine receptors, and how non-depolarizing muscle blockers cause paralysis. 2. Distinguish the prototype non-depolarizing blocking drugs based upon the clinical pharmacology. 3. Describe the mechanism of action of succinylcholine, list its primary clinical uses, and its contraindications. 4. List the prototype agents used to reverse neuromuscular blockade and to describe the physical signs of inadequate and ina

1
Q

primary NT at the NMJ

A

ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ACh must bind to _______ at the motor end plate to open the Na+ channel

A

BOTH a alpha subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

size and ionization of NMBs

A

large molecules, highly ionized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

effect of size of NMB molecules on CNS

A

large molecules cannot pass through BBB, therefore cannot act on CNS. Therefore can result in awake, paralyzed pt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

onset of action of NMB

A

slow (2-5 minutes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how to decrease onset time of NMBs

A

multiple ED95 dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how to prolong the duration of NMB

A

multiple ED95 dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

can effect kinetics of NMBs

A

age, other drugs, hepatic/renal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

prototype non-depolarizing locking drug (NDBD)

A

d-tubocurare (d-TC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

MOA of d-TC

A

reversible (competitive) binding to ACh receptor on a subunit (only needs to bind to 1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

prototype sterolidal NMB

A

vecuronium and rocuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

advantages of sterodial NMB

A

stable hemodynamics, duration not affected by renal dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

SE of vercuronium

A

associated with prolonged blockage in ICU pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

SE rocuronium

A

associated with occasional prolonged duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

longest acting, least expensive NMB

A

pancuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pancuronium shows prolonged action in ___ pts

A

renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

pancuronium has profound dependance on:

A

renal metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

NDBD that is sympathonimetic

A

pancuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

prototype Benzylisoquinolinium (BQ) drugs

A

cis-atracurium, mivacurium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

NDBD safe for renal/hepatic failure

A

BQ (cis-atracurium, mivacurium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

NMB that can be inactivated by high ambient temps

A

BQs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

side effect of Mivacurium

A

can cause histamine release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

NMB that may not require reversal

A

mivacurium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

can cause prolonged blockade in mivacurium and/or Sch

A

plasma cholinesterase insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
prototype depolarizing agent
Succinylcholine (Sch)
26
MOA of Sch
depolarizes membrane by opening Na+ channels by binding both a - subunits
27
drug that causes fasciculations
Sch
28
drug that causes flaccid paralysis
Sch
29
cause of Sch termination of action
redistribution away from motor end plate, and/or matabolized by plasma cholinesterase
30
NMD metabolized by plasma cholinesterases
Sch
31
effect of deficiency of plasma cholinesterases on Sch
prolonged blockade
32
advantages of Sch
rapid onset (30 seconds)
33
clincal use of Sch
rapid intubation/ intubation of trauma pts with full stomachs
34
NMD with shortest duration of action
Sch
35
NMD that causes hyperkalemia
Sch
36
drug that can cause post op myalgia, increased IOP/ICP/IGP
Sch
37
drug that can cause malignant hyperthermia
Sch
38
drug not reversiable with anticholesterase drugs
Sch
39
NMB drug that can cause cardiac arrythmias
Sch
40
how Sch can cause arrythmias
Sch mimics ACh at cardiac muscarinic receptors
41
why is NMB montoring essential?
clinical accumen not always accurate
42
method for monitoring NM blockade
evoked stimulatory response
43
areas for testing NM blockade stimulation
ulnar nerve, facial nerve, posterior tibial nerve
44
drug causing phase 1 blockade
Sch
45
drug(s) causing phase 2 blockade
all of them
46
phase of blockade with an antidote
phase 1
47
type of blockade in phase 1
prolonged blockade
48
type of blockade in phase 2
repolarized, but blocked
49
antidote for phase 2 blockade
cholinesterase inhibitors
50
ways to measure blockade
subjective/objective/ assement of evoked responses and clinical assesment of muscle strenght
51
signs of residual blockade/inadequate reversal
strong hand grip that weakens, and jerky movement
52
NMB only anethetic drugs that are:_____
routinely antagonized with pharmacologic reversal agents
53
common (3) NMB reversal agents
neostigmine, edrophonium, pyridostigmine
54
MOA of blockade reversal agents
inhibition of ACh-esterase, increases synaptic ACh concentrations
55
short onset blocking reversal agent
edrophonium
56
longest onset blocking reversal agents
pyridostigmine
57
side effects of NMB reversal agents
bradycardia, icnreased secretions, post-op N/V
58
drug given with NMB reversal agents to attenuate side effects
atrooine (edro) or glycopyrrolate (___stigmines)
59
when are anticholinesterase drugs contraindicated
absence of measurable responses to muscle stimulation
60
inadequate reversal can lead to:
residual neuromuscular blockade (RNMB)
61
signs of RNMB
ventilatory insufficiency, insufficient airway protection, visual disturbances, inability to sit without assistance, facial weakness, systemic fatigue
62
inappropriate reversal of NMB results in
postop N/V, tachycardia or bradycardia, bronchial/nasal secretions, excess sweating (can mimic MI diaphoresis)
63
NDBD antagonist drug
sugammadex
64
MOA of sugammadex
binds rocuroum or vecurinium with high affinity in bloodstream
65
signs of malignant hyperthermia
rapid onset of tachycardia, hypercarbia, hypertension, rigidity, hyperthermia, acidosis
66
results of malignant hyperthmia if untreated
rhabdo, organ failure, death
67
triggers of malignant hyperthermia
inhaled anesthetics and Sch
68
pathophys of malignant hyperthermia
hypermetabolism due to exagerated release of Ca++ from sarcoplasmic reticulum
69
only drug treatment for malignant hyperthermia
dantrolene
70
MOA of dantrolene
binds ryanodine receptor, inhibiting release of Ca++ from SR

CNS I (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions