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Anesthesia Meds > Anesthesia Med Sheet MOA/INFO > Flashcards

Anesthesia Med Sheet MOA/INFO Flashcards

1
Q

Etomidate S/E, metabolism and other

A

CV stable, less myocardial depression than propofol

S/E: myoclonus/pain on injection, cv stable, epileptic foci

METABOLISM: plasma esterases and hepatic enzymes; a single induction dose may inhibit 11 BH leading to adrenocortical suppression

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2
Q

ketamine S/E, metabolism and other

A

hallucinations
increased CO
increased HR
increased salivation
decreased BP
analgesia

metabolism: liver cyp450; redistribution

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3
Q

methohexital/brevital S/E, metabolism, other

A

porphyria
do not give with asthma

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4
Q

propofol S/E, metabolism and other

A

pain on injection
no use in egg/soy allergy
antiemetic
decreases CV

metabolism: liver and lungs

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5
Q

midazolam S/E, metabolism and other

A

decreased respiration
amnesia
1/2 life: 1-4 hrs
H2O soluble
benzo

eliminated renal

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6
Q

dexmedetomidine info to know

A

alpha 2 agonist

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7
Q

succinylcholine S/E, metabolism, other

A

short-acting depolarizing
can cause MH
locks NA channel

met: plasma pseudocholinesterase

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8
Q

mivacurium info to know

A

short-acting non depolarizing

met: plasma cholinesterase

can cause histamine release

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9
Q

atracurium info to know

A

intermediate acting nondepolarizing

metabolism: hoffman/ ester hydrolysis

can cause histamine release

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10
Q

vecuronium info to know

A

intermediate acting; nondepolarizing

metabolism: liver>kidney

high lipid solubility

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11
Q

rocuronium info to know

A

intermediate acting; nondepolarizing

metabolism: liver >kidney

painful on injection
shortest acting NDNMB

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12
Q

ciastracurium info to know

A

intermediate acting; nondepolarizing

met: hoffman/esterase hydrolysis

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13
Q

pancuronium info to know

A

long acting; nondepolarizing

metabolism: renal

increase HR- no NOREPI reuptake

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14
Q

fentanyl info to know

A

pulm 1st pass
can cause rigid chest

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15
Q

sufentanil info to know

A

can cause rigid chest
most potent
pulm 1st pass

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16
Q

remifentanil info to know

A

metabolized by hydrolysis esterase
ultra short acting
1/2 life: 6 min

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17
Q

meperidine info to know

A

metabolite = seizures
no with MAOIs
crosses placenta
increase HR
treats post op shivering

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18
Q

ketorolac info to know

A

bleeding/ inhibits COX

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19
Q

morphine info to know

A

can cause Nausea and vomitting
most allergies: +histamine
can cause biliary spasm

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20
Q

hydromorphone info to know

A

can cause N/V
+histamine
antitussive
1mg=7mg MSO4 (morphine sulfate)

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21
Q

etomidate MOA

A

GABA mimetic

binds to GABA receptor and enhances receptors affinity for GABA

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22
Q

Ketamine MOA

A

non competitively binds to NMDA (glutamate receptor)

inhibits glutamate receptor (excitatory)- decreases presynaptic release of glutamate and potentiates GABA release

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23
Q

methohexital MOA

A

barbituate

acts on GABA receptors

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24
Q

propofol MOA

A

modulates GABA receptors
increases transmembrane Cl- conduction- hyperpolarizes post-synaptic cell membrane
sedation and hypnosis

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25
Q

midazolam MOA

A

Works on the GABA receptor
To increases frequency of Cl-channel influx and
hyperpolarizes targeted cell

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26
Q

MOA of dexmedetomidine

A

Alpha 2 agonist

Binds with pre and postsynaptic alpha 2a agonist receptors

Decreases norepi levels; causes sedation and analgesia

Alpha 2 agonist
Decreases cAMP which inhibits the locus coeruleus in the pons = sedation

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27
Q

MOA of succinylcholine

A

Binds to one or both alpha subunits of nicotinic ACh receptors and mimics action of ACh

Depolarizes the membrane

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28
Q

MOA of mivacurium

A

binds competitively to cholinergic receptors to antagonize the action of ACh and cause neuromuscular blockade

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29
Q

MOA atracurium

A

reversibly competitive antagonism of ACh

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30
Q

MOA of vecuronium

A

reversibly competitive antagonism of ACh

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31
Q

MOA of rocuronium

A

reversibly competitive antagonism of ACh

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32
Q

MOA of cisatracurium

A

reversibly competitive antagonism of ACh

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33
Q

MOA of pancuronium

A

reversibly competitive antagonism of ACh

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34
Q

info about ephedrine

A

direct/indirect beta and alpha 1 agonist
can have tachyphylaxis
dont give with fast HR
dont give with MAOI
decreases uterine blood flow

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35
Q

info about phenylephrine

A

alpha 1 agonist
can cause reflex bradycardia (baroreceptor reflex)

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36
Q

info about epinephrine ( think hemodynamics)

A

direct beta1, beta2, alpha 1 agonist
causes increased CO
increased HR
increased contractility
increased SVR

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37
Q

info about dopamine

A

alpha1, beta1,beta2 and dopamine (renal perfusion) receptor agonist

avoid with MAOIs
400mg/250ml bag= 1600mcg/ml

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38
Q

info about dobutamine

A

selective beta1
inotrope

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39
Q

info about atropine

A

increases HR
causes mydriasis (pupil dilation)
tertiary ammonium (crosses BBB)

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40
Q

info about glycopyrrolate

A

decreases secretions
quaternary ammonium (DOES NOT CROSS BBB)

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41
Q

info about neostigmine

A

max dose 5mg
cholinergic syndrome
decreases HR
hepatic metabolism

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42
Q

info about physostigmine

A

crosses BBB (tertiary amine)
dont give with asthma
renal excreted

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43
Q

info about edrophonium

A

do not give with glycopyrrolate
renal excreted
can diagnose MG true reversible

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44
Q

info about flumazenil

A

benzo antagonist
repeat 0.2mg q 1min (3mg/hr max)

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45
Q

info about naloxone

A

reversal for opioids

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46
Q

info about hydralazine

A

Arteriole vasodilation causes increased cGMP
increased HR
increased CO
decreases SVR
increased RENIN

DOC with normal to low HR (beta blockers preferred for HTN with increased HR)

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47
Q

info about labetalol

A

alpha, beta1, beta2 antagonist
ratio 1:7 alpha to beta IV
decreases HR, give slow

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48
Q

info about esmolol

A

beta1 antagonist

metabolized by plasma hydrolysis

t1/2 9min

49
Q

info on ondansetron

A

5HT3 antagonist
admin slowly to prevent headache

50
Q

info about droperidol

A

paradoxical reaction( restless anxious)
decreases BP
change in dopamine in CNS (dont give with parkinsons)

51
Q

info about dexamethasone

A

decreases inflammation
decreases immunity

52
Q

muscarinic effects

A

decrease HR
bronchoconstriction
increased salivation
decreased BP
MIOSIS (pupil constriction)
intestinal spams

53
Q

MOA of fentanyl

A

opioid mu receptor agonist

54
Q

MOA of sufenta

A

opioid mu receptor agonist

55
Q

MOA of ultiva/remifentanil

A

opioid mu receptor agonist

56
Q

MOA of meperidine

A

synthetic opioid agonist at mu and kappa receptors

57
Q

MOA of toradol

A

nonselective NSAID
inhibits COX1 and COX2

58
Q

MOA of morphine

A

mostly mu agonist

inhibits ascending pain pathways

59
Q

MOA of hydromorphone

A

mostly mu agonist and some kappa receptors

60
Q

MOA of ephedrine

A

direct: alpha and beta agonist
indirect: causes release of endogenous catecholamines stored in nerve terminals

61
Q

MOA of epinephrine

A

beta 2> beta1> alpha1
beta1: inotropy, chronotropy
beta2: vasodilation (skeletal muscles) and bronchodilation
alpha1: vasoconstriction

62
Q

MOA of dopamine

A

adrenergic agonist
inotropic
precursor to norepi
alpha1, beta1, beta2, dopaminergic

63
Q

MOA of atropine

A

inhibits postganglionic muscarinic receptors
competes with ACh at the muscarinic receptor sites as an antagonist
increases firing of SA node and conduction through the AV node by blocking the action of the vagus nerve

64
Q

MOA of glycopyrrolate

A

competitively antagonizes ACh at muscarinic receptors

65
Q

MOA of bridion/sugammadex

A

noncovalently binds to the steroidal muscle relaxant
prevents NDNMBs from binding to nicotinic ACh
immediate reversal of NDNMB

66
Q

MOA of neostigmine

A

-anticholinesterase- accumulation of ACh at nicotinic receptors in NMJ
-does this by the formation of carbamyl esters
-reverses and restores neuromuscular transmission

67
Q

MOA of physostigmine

A

-anticholinesterase- increases ACh at nicotinic receptors in NMJ
-does this by formation of carbamyl esters
-more neurotransmitters available for interaction with cholinergic receptors

68
Q

MOA of edrophonium

A

anticholinesterase-

competitive inhibition through electrostatic attachment to the anionic site on the acetylcholinesterase enzyme (presynaptic)

69
Q

MOA of flumazenil

A

competitive GABA antagonist

prevents or reverses effects of benzos

70
Q

MOA of naloxone

A

competitively antagonizes mu, kappa, delta opioid receptors

greatest affinity for MU

71
Q

MOA of hydralazine

A

activates guanylate cyclase
increases cGMP
decreases intracellular Ca
ateriolar relaxation

72
Q

MOA of labetalol

A

selective alpha 1
nonselective beta1 and beta 2 blocker

73
Q

MOA of esmolol

A

selective B1 blocker

74
Q

MOA of ondansetron

A

5HT3 antagonist
blocks serotonin centrally at the CRTZ and peripherally

75
Q

MOA of droperidol

A

butyrophenone
dopamine antagonist at GABA in CRTZ

76
Q

MOA of dexamethasone

A

-glucocorticoid steroid
-derivative of prednisolone
-reduces surgery-induced inflammation due to inhibition of prostaglandin synthesis

77
Q

what medication has less myocardial depression than propofol

A

etomidate

78
Q

what medication can lead to adrenocortical suppression

A

etomidate

79
Q

what are some CV considerations of etomidate

A

CV stable
less myocardial depression than propofol

80
Q

what are side effects of etomidate

A

myoclonus
pain on injection
epileptic foci

81
Q

how is etomidate metabolized

A

plasma esterases and hepatic enzymes

82
Q

how does etomidate cause adrenocortical suppresssion

A

inhibits 11 beta hydroxylase

83
Q

what does ketamine do to HR, CO and BP

A

HR increases
BP decreases
CO increases

84
Q

what is a metabolism consideration with ketamine

A

redistribution

85
Q

what are 3 side effects of ketamine

A

hallucinations
analgesia
increase salivation

86
Q

what are the contraindications off methohexital

A

porphyria
asthma

87
Q

what are signs and symptoms of porphyria

A

hyponatremia
peripheral neuropathy
severe abdominal pain
psych problems

88
Q

where is propofol metabolized

A

lungs and liver

89
Q

how is versed eliminated

A

renal

90
Q

what is the half life of versed

A

1-4 hrs

91
Q

is versed water soluble

A

yes

92
Q

what are the short NMBs

A

succs
mivacurium

93
Q

what are the intermediate NMBs

A

atracurium
vec
roc
cisatracurium

94
Q

what is the long action NMB

A

pancuronium

95
Q

what is the shortest onset non depolarizing muscle blocker

A

roc

96
Q

what are considerations for succinylcholine?

A

metabolized by plasma pseudocholinesterase

locks sodium channel

can cause MH

97
Q

what is the specific temperature and pH called that causes spontaneous degradation of atracurium

A

hofman elimination

98
Q

what two NDNMB increase histamine release

A

mivacurium
atracurium

99
Q

what two NMB are eliminated by Hofman elimination or ester hydrolysis

A

cisatracurium
atracurium

100
Q

what are considerations for vecuronium

A

metabolized more in liver than kidney
increased lipid solubility

101
Q

what are considerations for rocuronium

A

metabolized more in liver than kidney
painful injection
shortest onset NDNMB

102
Q

what are considerations for pancuronium

A

increases HR
blocks norepi reuptake
eliminated in the kidneys

103
Q

what are considerations for fentanyl

A

rigid chest
pulmonary 1st pass effect

104
Q

what is pulmonary 1st pass effect

A

loss of drug on first circulation through the lungs

105
Q

what are considerations for giving sufentanil

A

rigid chest
pulm 1st pass effect
MOST POTENT

106
Q

what are considerations for remifentanil

A

ultra short acting
6.5 min half life
metabolized by hydrolysis esterase

107
Q

what are considerations for merperidine

A

DO NOT GIVE WITH MAOIs
crosses placenta
metabolite can cause seizures
increase HR
used for post op shivering

108
Q

what bp med is selective b1 and a positive inotrope

A

dobutamine

109
Q

what are considerations for ephedrine admin

A

does not increase uterine blood flow
direct/indirect betal and alpha1

110
Q

what should be done after admin of sugammadex

A

ptc
postetanic count aka twitches

111
Q

what side effects should you look for with neostigmine

A

cholinergic syndrome
decreased HR

112
Q

what class of drug is famotidine

A

H2 receptor antagonist

113
Q

MOA of famotidine

A

H2 receptor antagonist that produces selective and reversible inhibition of H2-mediated secretion of hydrogen ions produced by the stomach

114
Q

what is half life and peak of famotidine

A

half life: 2.5-4 hrs
peak: 1-3.5 hrs

115
Q

What NDNMB are supplied in 10mg/ml

A

Atracurium
Rocuronium

116
Q

What NDNMBs are supplied in 2 mg/ml

A

Mivacurium
Cisatracurium

And sometimes pancuronium

117
Q

What NDNMBs are supplied in 1mg/ml

A

Pancuronium
Vecuronium

118
Q

Edrophonium MOA

A

Anticholinesterase

Competitive inhibition through electrostatic attachment to the anionic site on the acetylcholinesterase enzyme (presynaptic)

119
Q

MOA of phenylephrine

A

directly activates alpha1
constricts arteries and veins
Veins>arteries
alpha 1>alpha2

Anesthesia Meds (7 decks)

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