Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MSC/Rheum/Derm > NMBs > Flashcards

NMBs Flashcards

1
Q

non-depolarizing types

A

isoquinoline derivatives

steroid derivatives

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

isoquinoline derivatives

A

atracurium
cisatracurium
D-tubocurarine

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

steroid derivatives

A

pancuronium
rocuronium
vecuronium

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

depolarizing agents

A

succinylcholine

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

reversal agents

A

edrophonium
pyridostigmine
neostigmine
sugammedex

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

nondepolarizing blocker MOA

A

prevents opening of AchR Na channel

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

depolarizing blocker MOA

A
  • initially opens AchR Na gate, causing depolarization

- persists on receptor binding site to physically block opened Na channel

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

metabolism

A

hepatic (faster) & renal

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

duration

A

correlates w/ t1/2

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

atracurium metabolism

A

hepatic metabolism produces laudanosine

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

why is laudanosine bad?

A

causes seizures

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

why is cisatracurium better than atracurium?

A

less dependent on hepatic inactivation, so less laudanosine produced, so less ADEs (seizures)

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

succinylcholine duration

A

5-10 min

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

succinylcholine metabolism

A
  • hepatic: butyrylcholinesterase

- plasma: pseudocholinesterase

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

variant pseudocholinesterase activity assay

A
  • colorimetric assay w/blood & dibucaine (enzyme inhibitor)
  • Acholest Test Paper
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

succinylcholine off target actions

A

stimulates:

  • ganglia (initially)
  • cardiac M receptors
  • histamine release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

drugs stimulating histamine release

A

succinylcholine

atracurium

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

drugs having effect on cardiac M receptor

A

succinylcholine (stimulation
pancuronium (moderate block)
rocuronium (slight)

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

succinylcholine ADEs

A 
hemodynamic changes
hyperkalemia in certain conditions
prolonged meuromuscular blockade 
increased IOP
muscle pain
myoglobinuria
malignant hyperthermia
anaphylaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hemodynamic changes

A

bradycardia or tachycardia.. nbd
ventricular arrhythmias
HTN

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

conditions causing hyperkalemia w/succinylcholine

A 
large burn injuries
trauma
massive crush injuries
upper&lower motor neuron injuries
muscular dystrophies
prolonged immobilization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

mechanism of hyperkalemia w/succinylcholine

A

up regulation of AchR or additional expression of two new isoforms of AchR
depolarization of AchR causes K+ efflux from muscle

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

mechanism of muscle pain w/succinylcholine

A

results from the initial stimulation of muscle fibers (fasciculations)

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

mechanism of malignant hyperthermia w/succinylcholine

A

uncontrolled release of Ca2+ from SR generates heat (as well as rigor, CO2, and lactate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Rx for malignant hyperthermia
``` **dantrolene** stop giving trigger agent hyperventilate w/O2 avoid CCBs correct hyperkalemia & acidosis cool core temperature ```
26
drugs that interact w/neuromuscular fxn
volatile anesthetics antibiotics local anesthetics other NMBs
27
NMBs act on which receptor?
Nm receptor
28
how do antibiotics interact with NMBs?
enhance blockate via depressed ACH release (pre-junctional P-type Ca2+ channels) (similar to effect of magnesium)
29
how do local anesthetics interact with NMBs?
depress neuromuscular fxn via pre-junctional neural effect (act on neuron, not at end plate)
30
how to antagonize phase I of succinylcholine effect?
small dose of non-depolarizing blocker
31
do NMBs result in complete paralysis?
nopeeee
32
how many twitches do we want when when dosing NMBs?
2or3 out of 4
33
how many receptors occupied by NMBs cause only first twitch?
85-90%
34
how many receptors occupied by NMBs to reach ideal dosing?
70-85%
35
ways to terminate NMBs
increase ACH levels | NMB encapsulation
36
ACHase inhibitors
neostigmine edrophonium pyridostigmine
37
do the ACHase inhibitors cross the BBB?
nopeeee
38
why do we get a second twitch that fades?
1) each activation depletes ACH 2) ACH acts on presynaptic nicotinic receptor for feedback amplification, prepares endplate for more signals, but LOLOL these are blocked by NMBs so you don't get amplification = subsequently less availability of ACH
39
what do we combine with ACHase inhibitors?
anticholinergics
40
and WHY do we combine drugs with ACHase inhibitors?
to reduce consequences of off-target activation
41
signs of increasing blockade
uhhh see sweatman's slide
42
combine neostigmine w/
glycopyrrolate
43
combine edrophonium w/
atropine
44
combine pyridostigmine w/
glycopyrrolate | but like.. don't remember this b/c its not used
45
other drugs linked to malignant hyperthermia
volatile anesthetics
46
ADEs w/atropine
tachycardia [bronchodilation] [antisialogogue]
47
ADEs w/scopolamine
sedation | antisialogogue
48
ADEs w/glycopyrrolate
antisialogogue [tachycardia] [bronchodilation]
49
da fuk is antisialogogue (don't even try to pronounce it Annie)
diminished/stopped saliva production, stops you from drooling (can we have this for desk naps)
50
off-target effects of ACHase inhibitors
``` CV: bradycardia, dysrhythmias Pulm: bronchospasm, increased secretions Brain: diffuse excitation (!!!) GI: increased peristalsis and secretions GU: increased bladder tone Eyeballs: pupillary constriction (miosis) ```
51
sugammadex MOA
encapsulates steroids reverses any depth of neuromuscular blockade inactive against non-steroidal NMBs
52
sugammadex structure
pore structure into which the NMB inserts
53
short procedures use
succinylcholine
54
long procedures use
steroidal or isoquinolone drugs
55
NMB ROA
IV
56
do NMBs reduce pain or anxiety?
NO DON'T BE DUMB
57
phase I of succinylcholine action
fasciculations
58
phase II of succinylcholine action
flaccid paralysis
59
ACHase inhibition effect on phase I
augments (more contraction)
60
ACHase inhibition effect on phase II
reverses or antagonizes (b/c competitive binding to AchR)

MSC/Rheum/Derm (2 decks)

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