NMB Flashcards

1
Q

fade during TOF is caused by

A

antagonism of pre-synaptic nicotinic receptors

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2
Q

acetylcholine - autonomic nervous system - which branch?

A

both! SNS and PNS but mostly Parasympathetic

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3
Q

how do depolarizing NMB’s work

A

depolarize the muscle fiber leaving it constantly stimulated and unable to be affected by Ach

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4
Q

how do non-depolarizers work

A

competitively block Ach from binding to receptors post-synaptically

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5
Q

non-depolarizers participate in ___ antagonism

A

competitive

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6
Q

ED95

A

dose of NMB necessary to produce 95% suppression of the single twitch response

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7
Q

ED95 when volatile anesthetic is used in conjunction with NMB

A

greatly reduced

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8
Q

use ___times the ED95 dose for tracheal intubation

A

2

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9
Q

which muscles are blocked first

A

small rapidly moving muscles - eyes and fingers

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10
Q

which muscle is blocked last

A

abdomen (diaphragm)

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11
Q

which muscle is a good predictor of laryngeal relaxation?

A

orbicularis

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12
Q

which muscles recover first?

A

larger muscles because they have more blood flow. (recovery in reverse order than paralysis)

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13
Q

ach channels are

A

ligand gated ion channels.

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14
Q

___% suppression of single twitch response is adequate for surgery

A

90

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15
Q

which non-dolparizers have a higher incidence of histamine release

A

benzylisoquinolinium

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16
Q

quaternary ammonium are ionized or lipophilic?

A

highly ionized.

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17
Q

quaternary cns effects?

A

none

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18
Q

quaternary binds to alpha sub unit ___ synaptically

A

post

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19
Q

quaternary are not completely specific, meaning they bind to

A

cardiac muscarinic and autonomic ganglia nicotinic

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20
Q

are quaternary’s highly protein bound?

A

no

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21
Q

which non-depol are long acting

A

panc, dox, and pipe

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22
Q

which non-depol are intermediate acting

A

atra, vec, roc, cis

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23
Q

which non-depol are short acting

A

miv

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24
Q

onset of succs

A

30-60s

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25
Q

duration of succs

A

3-5min

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26
Q

succs MOA

A

binds to one or both alpha subunits at nicotinic receptor. mimics Ach

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27
Q

does succs have a shorter or longer duration than ach

A

longer

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28
Q

succs increases K by

A

.5meq/L

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29
Q

tof ratio for succs

A

> 0.7

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30
Q

which recovers first.. diaphragm or peripheral muscles?

A

diaphragm

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31
Q

succs is broken down by

A

plasma cholinesterase in the blood

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32
Q

what things reduce the amt of plasma cholinesterase

A

severe liver dz, neostigmine, high estrogen levels. reglan

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33
Q

obese patients and cholinesterases

A

they have increased levels - so break down succs faster - need more

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34
Q

what kind of cardiac side effects does succs cause

A

arrhythmias - sinus brady, junctional rhythm, sinus arrest…. some people get tachycardia and inc BP due to ganglia stimulation (some people get sympathetic boost)

35
Q

what should you give to treat the bradycardia with succs?

A

epi. not atropine

36
Q

if something is anti-muscarinic, it is also

A

anticholinergic

37
Q

succs causes increased pressure where

A

intragastric, intraocular, intracrmail.

38
Q

which drug causes an increase in mortality for brain injured patients in the ED

A

succes

39
Q

what is the TOF ratio for non-depol

A

<0.7

40
Q

which ND’s cause histamine release

A

atra and miv

41
Q

panc CV effects

A

increased HR, MAP, CO. blocks vagal/muscarinic.. so anti-parasympathetic, SNS activation

42
Q

panc CV don’t give

A

digoxin

43
Q

critical myopathy is common with which class

A

aminosteroids , higher risk with corticosteroids

44
Q

critical myopathy what happens to pt’s

A

long term paralysis for mech vent >6 days

45
Q

NMB’s are enhanced by

A

volatile anesthetics, aminoglycosides, LA’s, antiarrhymics, diuretics, Mg, Li

46
Q

how do anticonvulsants affect NMB

A

affect cyp enzymes

47
Q

how does cyclosporine affect NMB

A

prolonged blockade

48
Q

how do corticosteroids affect NMB

A

compounded muscle weakness

49
Q

how do sympathomimetics affect NMB

A

increased onset d/t changes in blood flow. argument on whether it leads to shorter or longer duration.

50
Q

hypothermia ___ duration of NMB

A

prolongs

51
Q

how does HYPOkalemia affect NMB

A

resistance to succs and increases sensitivity to NDNMB

52
Q

how does HYPERkalemia affect NMB

A

increases succs effects and opposes NDNMB

53
Q

how does paresis or hemiplegia affect NMB

A

have extra junctional receptors so need more, mega doses

54
Q

are men or women more sensitive to NMB?

A

women

55
Q

long acting panc and pipe NDNMB’s have ___ positive nitrogens

A

2

56
Q

which long acting is a benzyl

A

dox

57
Q

panc structure

A

bisquaternary aminosteriod

58
Q

panc and renal failure

A

80% excreted unchanged in urine, renal failure reduces clearance up to 50%

59
Q

panc metabolite

A

3-desacetylpancuronium (half as potent as panc)

60
Q

how does liver disfunction effect panc

A

longer half life

61
Q

which NMB is enhanced by resp acidosis

A

panc

62
Q

ronium’s are

A

aminosteriods

63
Q

curium’s are

A

benzyl’s

64
Q

which NMB has an increased potency and shorter duration in infants

A

pipe

65
Q

which NDNMB have only 1 positive nitrogen and what does that do

A

vec and roc - lipophiilc.. hepatic/renal clearance.

66
Q

priming principle for roc

A
  1. small dose binds spare receptors, 4 min later deliver the rest.
67
Q

which NDNMB is 82% protein bound

A

atra

68
Q

which NDNMB’s undergo hoffman elimination

A

atra and cis

69
Q

hoffman elimination is accelerated by ___ and slowed by ____

A

alkalosis, acidosis

70
Q

which drugs have laudanosine as a metabolite

A

atra and cis. mostly atra - inactive at NMJ but may be CNS stimulant and increase MAC

71
Q

laudanosine causes peripheral ____ and ___ MAC of volatile anesthetics

A

vasodilation, increases

72
Q

atra CV

A

at 3x ED95 increase HR, decrease MAP. histamine release

73
Q

H1 and H2’s help with

A

histamine release with atra

74
Q

long term h2 blocker use may do what to CV effects of atra

A

exacerbate CV effects d/t histamine

75
Q

atra infant dose

A

half dose of older children

76
Q

cis main difference

A

no histamine release

77
Q

how is vec eliminated

A

both hepatic and renal. lipid soluble!

78
Q

vec and biliary excretion

A

40% unchanged in bile, exaggerated response with hepatic cirrhosis

79
Q

vec and urinary elmin

A

30% unchanged in urine, half life prolonged in renal failure

80
Q

cumulative effects of vec panc and atra

A

panc> vec> atra

81
Q

which has a slight vagolytic effect… vec or roc?

A

roc

82
Q

vec has a ___ onset in infants

A

rapid

83
Q

vec and elderly

A

decreased clearance, longer recovery

84
Q

onset of roc

A

1-2min