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Adv Pharm II > Exam 2: NMB, Reversals > Flashcards

Exam 2: NMB, Reversals Flashcards

1
Q

how many tof twitches need to be present before reversal drug is administered

A

1-2

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2
Q

what should tofr be to meet extubation criteria

A

0.7 or 0.9 depending on study

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3
Q

how long should tetany be to meet extubation criteria

A

5 seconds sustained at 50 hz

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4
Q

what are 2 other signs patient is a ready for extubation

A

strong constant hand grip
5 second head lift

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5
Q

what vital capacity suggests recovery from nmb

A

15ml/kg

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6
Q

what inspiratory force suggests recovery from nmb

A

-25-30 cmh2o
>-40

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7
Q

what is the goal of reversal drugs

A

maximize nicotinic transmission
minimize muscarinic SE

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8
Q

how many minutes need to be given for anticholinesterase inhibitors to fully antagonize nmb

A

15-30 min

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9
Q

what term is defined as a tofr less than 0.9

A

residual NMB

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10
Q

what is a drug class that can hinder the action of reversal agents thus prolonging nmb’s

A

aminoglycoside abx

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11
Q

what are three electrolyte imbalances that can influence reversal agents

A

hypermagnesemia
hypocalcemia
hypokalemia

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12
Q

besides certain drugs and electrolyte imbalances, what can affect reversal agents

A

depth of block at time of reversal
clearance/half life of reversal
resp acidosis
hypothermia

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13
Q

what can giving an excessive dose of acetylcholinesterase inhibitor cause

A

paradoxical muscle weakness

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14
Q

t or f- make sure to adjust dose of both ache inhibitors and nmb in patient with renal failure

A

f- do not adjust since doa of both is affected

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15
Q

t or f- neostigmine will take longer to reach peak effect with 90% twitch suppression when compared to 50% twitch suppression

A

true

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16
Q

t or f- ache inhibitors do not have a synergistic effect

A

false
Additive

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17
Q

how long can residual paralysis occur for after intermediate nmb

A

4 hrs

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18
Q

what is the term for when adequate dose of reversal is given, but blockade is re-established because reversal gets metabolized faster than nmb drug

A

recurarization

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19
Q

which receptors does ach agonize

A

nicotinic
muscarinic

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20
Q

which receptor do nondepolarizing agents antagonize

A

nicotinic receptors

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21
Q

which receptor does atropine/scopolamine/glycopyrrolate antagonize

A

muscarinic

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22
Q

what are two locations of nicotinic receptors

A

autonomic ganglia
skeletal muscle

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23
Q

what are two locations of muscarinic receptors

A

glands
smooth muscle (gi/bladder/bronchial)
heart

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24
Q

what drugs block muscarinic receptors

A

atropine, glycopyrolate

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25
Q

t or f- nicotinic and muscarinic receptors respond to ach

A

true

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26
Q

why are anticholinergic meds given with cholinesterase inhibitors

A

minimize muscarinic effects

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27
Q

what is a cv muscarinic se after anticholinesterase is given

A

bradycardia

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28
Q

what is a muscarinic se of lungs after reversal is given

A

bronchospasm
bronchial secretions

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29
Q

what is a cerebral muscarinic se after reversal is given

A

diffuse excitation

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30
Q

what is a gi muscarinic se after reversal is given

A

intestinal spasm
increased salivation

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31
Q

what is a gu muscarinic se after reversal is given

A

increased bladder tone

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32
Q

what is an ophthalmological muscarinic se after reversal is given

A

miosis

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33
Q

what is the action of cholinesterase inhibitors

A

indirectly increase ach to compete with non-depolarizing nmb

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34
Q

t or f- acetylcholinesterase inhibitors irreversibly bind to acetylcholinesterase

A

false
reversible

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35
Q

what is the supplied dose of neostigmine and physostigmine

A

1mg/ml

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36
Q

what is the reversal dose of neostigmine

A

0.05mg/kg

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37
Q

what is the onset, peak, and doa of neostig

A

3-5 mins, 7 mins, 1-2 hrs

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38
Q

what is max dose of neostig

A

5mg

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39
Q

how is neostig metabolized

A

liver

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40
Q

what is the structure of neostigmine and enlon

A

quaternary amine

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41
Q

t or f- neostig and enlon do not cross bbb

A

true

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42
Q

what are some side effects of neostig

A

ponv
pruritus
diarrhea
prolonged block

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43
Q

what do acetylcholinesterase inhibitors do to succ

A

prolong depolarization

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44
Q

what two meds inhibit pseudocholinesterase activity

A

neostig and physostig

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45
Q

what side effect should be watched for with neostig admin

A

cholinergic syndrome

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46
Q

what is the onset and doa of physostigmine

A

15 min, 2 hrs

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47
Q

How is physostigmine metabolized?

A

renal

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48
Q

what med is a tertiary amine and cross bbb

A

physostigmine

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49
Q

what reversal med should not be given with asthma

A

physostigmine

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50
Q

which reversal agent reduces post op shivering

A

physostigmine

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51
Q

what is the reversal dose for physostigmine

A

0.5-1mg
peds: 0.02 mg/kg

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52
Q

what is the supplied dose of enlon

A

10mg/ml

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53
Q

what is the reversal dose of enlon

A

0.5-1mg/kg

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54
Q

what is the onset, peak, and doa of enlon

A

30-60 sec
1 min
60 mins

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55
Q

where is the primary action of enlon

A

presynaptic

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56
Q

what is the most rapid acting cholinesterase inhibitor

A

enlon

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57
Q

t or f- enlon is recommended for a deep block

A

false

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58
Q

which should be given first, robinul or enlon and why

A

robinul- prevent bradycardia

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59
Q

what med is used to diagnose/treat myasthenia gravis

A

enlon

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60
Q

dumbbells

A

diarrhea
urination
miosis
bradyhcardia
bronchoconstriction
emesis
lacrimation
laxation
salivation

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61
Q

what are some side effects of antimuscarinics

A

tachyarrhythmias
nausea
constipation
dizziness

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62
Q

what med is a gamma cyclodextrin made of sugar that assembles in a ring

A

sugammadex

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63
Q

how does sugammadex work

A

encapsulates aminosteroid nmb making it inactive

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64
Q

what meds are sugammadex most effective for

A

roc, vec, pancuronium

book says roc and vec, higher affinity for roc

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65
Q

t or f- make sure to give antimuscarinic with sugammadex

A

f- you are not affecting acetylcholine

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66
Q

what are the uncommon se of sugammadex

A

anaphylaxis
bradycardia
decreased effect of hormonal birth control for 7 days

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67
Q

what are the pros of sugammadex

A

improves safety for rapid reversal
reduces risk of residual paralysis
allows for strong nmb until end of procedure

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68
Q

what is key before giving sugammadex

A

blockade depth monitoring

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69
Q

what is sugammadex dose for tof 2/4 or better

A

2mg/kg

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70
Q

what is sugammadex dose for tof of 0/4 and 2 ptc or better

A

4mg/kg

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71
Q

what is sugammadex dose after giving 1.2 mg/kg of roc

A

16 mg/kg

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72
Q

how long do you have to wait after giving roc to reverse

A

3 min

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73
Q

what is recommended med to give with neostig

A

glycopyrolate

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74
Q

what is recommended med to give with pyridostigmine

A

glycopyrolate

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75
Q

what is recommended med to give with enlon

A

atropine

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76
Q

what is the dose of atropine

A

7mcg/kg

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77
Q

what is the onset, peak and doa of atropine

A

1 min, 2min, 1 hour

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78
Q

what can very small doses of atropine cause

A

paradoxical bradycardia

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79
Q

which med is a tertiary ammonium

A

atropine

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80
Q

t or f- atropine cross bbb but not placenta

A

f- crosses both

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81
Q

what med is a quaternary ammonium and does not cross bbb

A

glycopyrolate

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82
Q

what is the dose of glycopyrolate

A

5-8 mcg/kg

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83
Q

what is the onset, peak, and doa of glycopyrolate

A

2-3 min, 5 min, 1-2 hours

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84
Q

which anticholinergic increases hr from most to least

A

atropine > glycopyrolate > scopolamine

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85
Q

what two anticholinergics cause the most smooth muscle relaxation

A

atropine, glyco

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86
Q

which anticholinergic causes sedation from most to least

A

scopolamine, atropine, glyco

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87
Q

which anticholinergic decreases saliva from most to least

A

scopolamine, glyco, atropine

88
Q

which anticholinergic prevents motion induced nausea from most to least

A

scopolamine, atropine, glyco

89
Q

which anticholinergic decreases gastric H secretion from most to least

A

all the same

90
Q

which anticholinergic causes mydriasis from most to least

A

scopolamine, atropine, glyco

91
Q

what rule states that volatile agents potency is proportional to their lipid solubility which is measured by oil gas partition coefficient

A

meyer-overton rule

92
Q

t or f- males have increased mac

A

false
gender has no effect

93
Q

what are some other factors that decrease mac

A

hypotension
hypoxia
anemia
metabolic acidosis
postpartum 1-3 days
paco2 > 95

94
Q

what drugs cause increased mac

A

chronic alcohol
acute amphetamine
maoi
ephedrine
levodopa

95
Q

what drugs cause decreased mac

A

acute alcohol
iv anesthetics
n2o
opioids
alpha 2 agonist
lithium
lidocaine
hydroxyzine

96
Q

how does age influence mac

A

increased in infants 1-6 months
>40= mac decreases 6% per decade

97
Q

what electrolyte abnormality will increase/decrease mac

A

increase: hypernatremia
decrease: hyponatremia

98
Q

what are some of the molecular targets of volatile anesthetics

A

gaba- enhance inhibitory
glycine- enhance inhibitory
k channels- activate
nmda- inhibit
nicotinic ach- inhibit
ca/na channels- inhibit

99
Q

what targets do volatiles enhance/activate

A

gaba
glycine
k channels- 2 pore and leak

100
Q

what targets do volatiles inhibit

A

nmda
nicotinic ach
na/ca channels

101
Q

t or f- nitrous oxide has a strong inhibitor action on nmda receptors

A

true

102
Q

why do we still give opioids with volatile anesthetics

A

volatiles have poor control of ans response to pain

103
Q

what does volatile blocking na/ca channels do

A

decreases action potentials/depolarizations

104
Q

where do volatiles cause unconsciousness in the brain

A

cerebral cortex
thalamus
brain stem

105
Q

t or f- volatiles cause amnesia

A

true

106
Q

t or f- immobility from volatile anesthetics is caused by enhancing gaba receptors

A

f- enhancing glycine receptors

107
Q

analgesia from volatiles is likely produced from disruption of ___________________ ____________ of pain transmission

A

spinothalamic tract

108
Q

immobility occurs from effects of inhaled anesthetic on __________ __________ networks

A

spinal cord

109
Q

what are the non-anesthetic effects of volatile gases

A

bronchodilation
neuromuscular effects
analgesia

110
Q

how do volatiles cause bronchodilation

A

-block calcium channels, deplete ca stores in sarcoplasmic reticulum
-potentiate gaba

111
Q

t or f- volatile anesthetics potentiate depolarizing and non-depolarizing nmb’s

A

true

112
Q

what is the neuromuscular effect of volatile gases

A

skeletal muscle relaxation

113
Q

which gas can have analgesic effects and how

A

nitrous oxide- nmda inhibitor

114
Q

what do volatiles do to cmro2

A

decrease

115
Q

what type of analgesia do volatile anesthetics provide

A

supraspinal

116
Q

what kind of toxicity can volatiles cause

A

hepatotoxicity
nephrotoxcity

117
Q

what are the adverse effect categories of volatiles

A

resp/cardiac depression
cardiac dysrhythmias
nephrotoxicity
MH
PONV

118
Q

how do volatiles cause resp depression

A

blunt hypoxic/hypercarbic vent responses for several hours

119
Q

how do volatiles cause cv depression

A

alter ca entry

120
Q

which volatiles decrease svr

A

iso, sevo, des

121
Q

which anesthetic has minimal cv effects

A

nitrous oxide

122
Q

what dysrhythmia can iso/sevo/des cause

A

long qt–>torsades

123
Q

which volatile does not contribute to MH

A

nitrous oxide

124
Q

what receptor is involved in MH

A

ryr1- releases a lot of calcium

125
Q

metabolism of sevo can lead to what

A

compound a- which is nephrotoxic

126
Q

how do volatiles cause nephrotoxicity and how

A

metabolism leading to inorganic fluoride production or by degradation products

127
Q

what can you substitute volatiles for to decrease ponv

A

prop

128
Q

which volatile is sweet smelling

A

sevo

129
Q

which volatile is half as potent as iso

A

sevo

130
Q

which volatile induces least amount of cerebral vasodilation

A

sevo

131
Q

which volatile has more favorable side effects

A

iso

132
Q

which volatile is highly pungent and chemically stable

A

iso

133
Q

what makes sevo better suited for inhalation inductions

A

minimally pungent

134
Q

which volatile can cause exothermic reactions with co2

A

sevo

135
Q

which volatile is a fluorinated methyl ethyl ether

A

des

136
Q

what effect does fluorination have on des

A

decreases potency

137
Q

which volatile has a low boiling point necessitating a specialized pressure vaporizer

A

des

138
Q

which volatile has almost no metabolism so there is decreased risk of hepto/nephrotoxicity

A

des

139
Q

which volatile is the most pungent

A

des

140
Q

which volatile causes coughing, breathing holding, laryngospasms

A

des

141
Q

which gas is technically not a volatile

A

N20

142
Q

which gas is an oxidizer that supports combustion

A

N20

143
Q

which gas has a low anesthetic potency

A

N20

144
Q

which gas should be avoided in first trimester of pregnancy

A

N20

145
Q

which gas promotes stable hemodynamics

A

N20

146
Q

which gas has an insufflation risk

A

n20

147
Q

which gas provides analgesia and euphoria

A

N2O

148
Q

what 4 factors influence mac

A

age
electrolytes
temp
genetic effects on potency

149
Q

opioids and volatiles have a ____________________ effect

A

synergistic

150
Q

t or f- there is synergism between inhaled anesthetics

A

false

151
Q

mac requirements __________________ with age

A

decline

152
Q

mac for inhaled anesthetic decreases with decreasing body temp by ___ to ___ % per 1 degree

A

4-5%

153
Q

which population needs for gas/adjuvants to reach 1 mac

A

pediatrics

154
Q

what cardiac problems can volatiles cause

A

coronary vasodilation which can lead to coronary steal

155
Q

what is the term for blood flow distal to atherosclerotic lesion decreases due to dilation, which then triggers ischemia

A

coronary steal

156
Q

which population can volatiles cause delayed neuronal development

A

neonates

157
Q

what are the primary binding sites for inhaled anesthetics

A

lipid and amphiphatic protein receptors

158
Q

which effect is not associated with fentanyl
a. vasodilation
b. resp depression
c. pruritis
d. vasoconstriction

A

vasoconstriction

159
Q

which of the following aretrue regarding zofran- Maman
a. risk for qt prolongation
b. headache is common se
c. ideally give dose pre-induction
d. 5ht3 agonist
e. all of the above

A

A
B

160
Q

which medication can cause transient htn after rapid admin
a. clonidine
b. precedex
c. decadron
d. droperidol

A

precedex

161
Q

how do you treat scopolamine anti cholinergic syndrome

A

physostigmine

162
Q

What conditions are contraindications for succs

A

Upper/lower motor neuron injury
Spinal cord injury
Burns
Skeletal muscle trauma
Cerebrovascular accident
Tetanus
Severe sepsis
Muscular dystrophy
Prolonged chemical denervation (magnesium, long term NMB infusion, clostridial toxin)

163
Q

what principle is the oil gas coefficient based on

A

meyer overton correlation

164
Q

which two volatiles are the same except for substituting a chloride for a fluorine atom

A

isoflurane and desflurane

165
Q

what correlation suggests that lipids were the principles target for anesthetics

A

meyer overton correlation

166
Q

which volatiles have a chiral carbon atom

A

isoflurane
desflurane

167
Q

what type of ion channels are though to be among the most relevant for general anesthetics

A

ligand gated
voltage gated

168
Q

what are the two suggested mechanisms of action for general anesthetics

A

lipid based
protein based

169
Q

according to the book, what three things compose anesthesia

A

reversible amnesia
loss of consciousness
immobility

170
Q

what are some receptors that volatiles enhance

A

gaba (inhibitory)
glycine (inhibitory)
nmda (inhibitory)
nicotinic ach
k channels

171
Q

what are some channels that volatiles inhibit

A

sodium
calcium

172
Q

immobility from volatiles is due to effects on _____________ __________ networks

A

spinal cord

173
Q

t or f- volatiles have good control of autonomic nervous system response to painful stimuli

A

false

174
Q

how is analgesia brought about by volatiles

A

disruption of spinothalamic tract transmission

175
Q

what receptor is likely acted on by volatiles to produce amnesia

A

GABA

176
Q

what area of the brain are gaba receptors likely acted on to produce amnesia

A

frontal cortex
hippocampus
amygdala

177
Q

t or f-nitrous oxide/xenon cause vasodilation and myocardial depression

A

false

178
Q

what types of organ toxicity can volatiles cause

A

hepatotoxicity
nephrotoxicity

179
Q

do volatiles cause bronchodilation or bronchoconstriction and how

A

bronchodilation- block calcium channels

180
Q

t or f- volatiles potentiate non depolarizing and depolarizing nmb’s

A

true

181
Q

which volatiles cause dose dependent respiratory depression

A

des
iso
sevo

182
Q

anesthetics reduce minute ventilation, does it do this by effecting tidal volume or respiratory rate

A

tidal volume

183
Q

which volatiles decrease carotid body response to hypoxia from most to least

A

halothane
isoflurane
des

184
Q

which gases have minimal direct cv effects

A

nitrous oxide
xenon

185
Q

which gas is reduced svr more prominent

A

isoflurane

186
Q

which gas promotes coronary steal in coronary artery disease

A

isoflurane

187
Q

rapid increases in what volatiles lead to increase in hr

A

isoflurane
desflurane

188
Q

which volatile has minimal effects on heart rate

A

sevo

189
Q

which gas increases cerebral blood flow and cmro2

A

N20

190
Q

what part of volatile gases produces nephrotoxicity

A

fluoride production

191
Q

seven side effects of Succs

A

bradycardia
tachycardia
K released
increased ocular pressure
increased ICP
increased intragastric pressure
MH

192
Q

why does succs cause bradycardia

A

stimulation of M2 receptor in SA node

193
Q

why does Succs cause tachycardia

A

mimics Ach at the sympathetic ganglia

194
Q

which enzymes hydrolyze succs

A

butyrylcholinesterase
psuedocholinesterase
plasma cholinesterase

195
Q

where is pseudocholinesterase produced

A

liver

196
Q

what factors prolong succs

A

reglan
late stage pregnancy
esmolol
oral contraceptives
echothiophate
cyclophosphamide
neostigmine

reduce psuedocholnesterase activity

197
Q

what conditions reduce psuedocholinesterase activity

A

atypical PChE
severe liver disease
burns
neoplasm
pregnancy (late stage)

198
Q

PChE variant typical homozygous dibucaine number and succs duration

A

70-80

duration: 5-10 min

199
Q

PChE variant heterozygous dibucaine number and succs duration

A

50-60

duration: 20-30 min

200
Q

PChE variant atypical homozygous dibucaine number and succs duration

A

20-30

duration: 4-8 hrs

201
Q

what primary event terminates rocuronium

A

biliary excretion/liver

APEX

202
Q

how is pancuronium terminated

A

renal excretion

203
Q

how is atracurium terminated

A

non specific ester hydrolysis

204
Q

how is cisatracurium terminated

A

hoffmann elimination

205
Q

what two NDNMBs dont produce a metabolite

A

roc
mivacurium

206
Q

what drugs/conditions potentiate neuromuscular blockade

A

desflurane
gentamycin
dantrolene
aminoglycocides
clindamycin
tetracycline
verapamil
LAs
furosemide
cyclosporin
increased lithium
increased Mg
decreased K and Ca
hypothermia

207
Q

why do NMB cause anaphylaxis

A

they contain one or more antigenic quaternary ammonium groups that interact with IgE causing mast cell and basophil degranulation

208
Q

which NMBs most likely to cause allergic reactions

A

succs
roc

209
Q

which reversal reduces post op shivering

A

physostigmine (40mcg/kg)

210
Q

what two reversals are best paired with glycopyrrolate

A

neostigmine
pyridostigmine

211
Q

which acetylcholinesterase inhibitor crosses the BBB

A

physostigmine

212
Q

most to least anticholinergic HR effects

A

atropine most
robinol
scopolamine least

213
Q

most to least anticholinergic effects on sedation

A

scopolamine most
atropine
robinol zero

214
Q

most to least anticholinergic antisialagogue

A

scopolamine most
robinol
atropine least

215
Q

which anticholinergics cross the BBB

A

atropine
scopolamine

Adv Pharm II (3 decks)

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