Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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
Q

Rx for malignant hyperthermia

A 
**dantrolene**
stop giving trigger agent
hyperventilate w/O2
avoid CCBs
correct hyperkalemia & acidosis
cool core temperature
26
Q

drugs that interact w/neuromuscular fxn

A

volatile anesthetics
antibiotics
local anesthetics
other NMBs

27
Q

NMBs act on which receptor?

A

Nm receptor

28
Q

how do antibiotics interact with NMBs?

A

enhance blockate via depressed ACH release (pre-junctional P-type Ca2+ channels) (similar to effect of magnesium)

29
Q

how do local anesthetics interact with NMBs?

A

depress neuromuscular fxn via pre-junctional neural effect (act on neuron, not at end plate)

30
Q

how to antagonize phase I of succinylcholine effect?

A

small dose of non-depolarizing blocker

31
Q

do NMBs result in complete paralysis?

A

nopeeee

32
Q

how many twitches do we want when when dosing NMBs?

A

2or3 out of 4

33
Q

how many receptors occupied by NMBs cause only first twitch?

A

85-90%

34
Q

how many receptors occupied by NMBs to reach ideal dosing?

A

70-85%

35
Q

ways to terminate NMBs

A

increase ACH levels

NMB encapsulation

36
Q

ACHase inhibitors

A

neostigmine
edrophonium
pyridostigmine

37
Q

do the ACHase inhibitors cross the BBB?

A

nopeeee

38
Q

why do we get a second twitch that fades?

A

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
Q

what do we combine with ACHase inhibitors?

A

anticholinergics

40
Q

and WHY do we combine drugs with ACHase inhibitors?

A

to reduce consequences of off-target activation

41
Q

signs of increasing blockade

A

uhhh see sweatman’s slide

42
Q

combine neostigmine w/

A

glycopyrrolate

43
Q

combine edrophonium w/

A

atropine

44
Q

combine pyridostigmine w/

A

glycopyrrolate

but like.. don’t remember this b/c its not used

45
Q

other drugs linked to malignant hyperthermia

A

volatile anesthetics

46
Q

ADEs w/atropine

A

tachycardia
[bronchodilation]
[antisialogogue]

47
Q

ADEs w/scopolamine

A

sedation

antisialogogue

48
Q

ADEs w/glycopyrrolate

A

antisialogogue
[tachycardia]
[bronchodilation]

49
Q

da fuk is antisialogogue (don’t even try to pronounce it Annie)

A

diminished/stopped saliva production, stops you from drooling (can we have this for desk naps)

50
Q

off-target effects of ACHase inhibitors

A 
CV: bradycardia, dysrhythmias 
Pulm: bronchospasm, increased secretions
Brain: diffuse excitation (!!!)
GI: increased peristalsis and secretions
GU: increased bladder tone
Eyeballs: pupillary constriction (miosis)
51
Q

sugammadex MOA

A

encapsulates steroids
reverses any depth of neuromuscular blockade
inactive against non-steroidal NMBs

52
Q

sugammadex structure

A

pore structure into which the NMB inserts

53
Q

short procedures use

A

succinylcholine

54
Q

long procedures use

A

steroidal or isoquinolone drugs

55
Q

NMB ROA

A

IV

56
Q

do NMBs reduce pain or anxiety?

A

NO DON’T BE DUMB

57
Q

phase I of succinylcholine action

A

fasciculations

58
Q

phase II of succinylcholine action

A

flaccid paralysis

59
Q

ACHase inhibition effect on phase I

A

augments (more contraction)

60
Q

ACHase inhibition effect on phase II

A

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