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Lindsays Flashcardlet > RE Ch 9 > Flashcards

RE Ch 9 Flashcards

0
Q

The time to awakening following a single dose of propofol is generally how long?

A

5-15 minutes

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1
Q

An open vial of propofol is good for how long?

A

12 hours, or 6 hours if transferred from its original container- like in a syringe

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2
Q

True or False: Metabolism of propofol plays the biggest role in initial awakening of the patient, but little in the eventual clearance of the drug.

A

FALSE
Metabolism plays little role in the initial awakening
Metabolism IS important in the eventual clearance of the drug

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3
Q

True or False. Propofol has rapid metabolic clearance which actually exceeds hepatic blood flow.

A

TRUE

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4
Q

Why might you see no change in elimination for patients with severe cirrhosis?

A

Likely due to extrahepatic sites of metabolism

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5
Q

What percent of propofol is excreted unchanged?

A

1%

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6
Q 
which enzyme is not responsible for the metabolism of propofol
CYP2B6
UGTHP4
CYP2C6
CYP450
A

CYP450

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7
Q

While the dose of propofol is decreased for the elderly, why is it increased for children?

A

they have an increased volume of distribution based on body weight and their rate of clearance is also higher

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8
Q

The elimination half life of propofol is how long

A

1-2 hours

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9
Q

Propofol reversibly binds to _____________ (50%) and _________ (48%) which makes the free concentration less than 2%.

A 
erythrocytes
plasma proteins (most commonly plasma albumin)
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10
Q

Define decrement time

A

time from the end of the infusion to 50% recovery and includes pharmacokinetic data related to concentration decrease and pharmacodynamic data correlating with recovery.

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11
Q

Three scenarios that may increase the level of free active fraction

A

third trimester pregnancy
kidney failure
liver failure
all cause decreased plasma protein levels

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12
Q

The GABAa receptor where propofol works is what type of receptor

A

Ligand-gated ion channel receptor is activated by binding of the neurotransmitter GABA

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13
Q

The binding of GABA to GABAa receptors initiates the movement of what ion through ion channels into the cell?

A

chloride

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14
Q

The movement of chloride into the cell results in what?

A

hypopolarization of postsynaptic cell membrane and the inhibition of neuronal cell excitation.

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15
Q

True or false: propofol both directly stimulates GABAa receptors AND potentiates the actions of endogenous GABA.

A

TRUE

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16
Q

Name 4 dose dependent physiologic reductions that occur with propofol infusions.

A

CBF
CMRO2
ICP
CPP

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17
Q

True or False: Cerebral auto-regulation and reactivity to changes in CO2 are preserved with propofol.

A

True

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18
Q

propofol causes cerebral vasodilation or constriction?

A

vasoconstriction (pg 107)

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19
Q

Propofol may cause insignificant hypotension in healthy adults and children. Predictors of hypotension with propofol induction are….

A

age greater than 50
ASA class 3 or 4
baseline MAP less than 70
coadministration with high dose fentanyl

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20
Q

List the factors from table 9-3 that alter protein binding
Increase binding:
Decrease binding:

A

Increase: increased pH >8.0, Increased protein concentration

Decrease: Decreased lipid solubility, Increased drug concentration, Increased competition for binding sites with other drugs

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21
Q

Propofol induced hypotension results from a combination of….

WHAT ARE THE PRIMARY REASONS?

A

a combination of CNS,cardiac, and baroreceptor depression, as well as decreases in sympathetic tone and systemic vasodilation

PRIMARY- DECREASED SYMPATHETIC TONE AND VASODILATION

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22
Q

Can propofol be used in cardiac anesthesia?

A

Yes, but with a decreased dose

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23
Q

With propfol administration- which is greater….decrease in tidal volume or decrease in resp rate?

A

Tidal volume. although apnea is common with initial or induction dose

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24
Q

Does propofol cause histamine release?

A

No

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25
Q

which anesthetic agent is NOT a preferred induction agent for a patient with asthma?
Propofol
Ketamine
Etomidate

A

Etomidate

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26
Q

Does propofol cross the placenta in pregnant women? give rationale

A

Yes, propofol is highly lipid soluble and therefore DOES cross the placenta often leading to neonate sedation and lower apgar scores

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27
Q

what is the ph and pka of etomidate

A

8.1 and 4.2

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28
Q

advantages and disadvantages of etomidate

A

no cardiac or respiratory effects

nausea, vomiting, pain with injection, no analgesia, adrenocortical suppression, myoclonia

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29
Q

Induction dose of etomidate

A

0.2-0.3 mg/kg

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30
Q

How is etomidate metabolized?

A

rapidly metabolized by the liver by hepatic microsomal enzymes and plasma esterases

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31
Q

what is the primary mode of metabolism of etomidate

A

ester hydrolysis in liver and plasma

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32
Q

etomidate is eliminated where?

A

10% bile
13% feces
remainder kidneys

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33
Q

T or F rapid metabolism accounts for etomidates extremely short duration of action?

A

F- Rapid Redistribution accounts for extremely short DOA

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34
Q

etomidate is or is not lipid soluble?

A

it IS lipid soluble so within a minute of administration brain levels rise rapidly.

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35
Q

What is the hepatic extraction ratio of etomidate?

what is the terminal half life

A

67%

2-5 hours

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36
Q

describe etomidates protein binding

A

76% protein bound, mostly to albumin

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37
Q

two factors that may compensate for changes in protein binding of etomidate?

A

metabolism and elimination

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38
Q

What is the MOA of etomidate?

A

GABA modulation

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39
Q

Cerebral blood flow and CMRO2 are increased or decreased by etomidate?

A

decreased

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40
Q

etomidate will increase or decrease intraocular pressure

A

decrease

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41
Q

pretreatment with which drugs may reduce the incidence of etomidate induced myclonia?

A

precedex, roc, lidocaine, midaz, or a small dose of etomidate prior to the induction dose.

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42
Q

which population is likely to have a significant decrease in sbp, pap, and pcwp following etomidate administration.

A

pts with aortic and mitral valve disease

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43
Q

describe the dose dependent changes seen with etomidate in regards to minute ventilation and respiratory rate

A

Ve decreases

RR increases

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44
Q

The ventilatory response to CO2 following etomidate administration is increased, decreased, or unchanged?

A

decreased

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45
Q

Enzymes inhibited responsible for the adrenocortical suppression seen with etomidate induction

A

The P450 dependent enzymes and 11B-hydroxylase

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46
Q

The inhibition of those enzymes results in an increase in _______ and decrease in ________.

A

cortisol precursors

cortisol, aldosterone, and corticosterone levels

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47
Q

solvent that causes pain and phlebitis on injection of etomidate

A

propylene glycol

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48
Q

3 contraindications of etomidate

A

known sensitivity
adrenal suppression
acute porphyrias

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49
Q

induction agents safe to use with patients with acute porphyria

A

propofol

ketamine

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50
Q

MOA of etomidate appears to be

A

GABA-mimetic

51
Q

Due to the inhibition of 11B-hydroxylase which is required for the production of both corticosteroids and mineralocorticoids clinically significant reduction in ___________ may result from using etomidate both single dose and infusion

A

steroid production

52
Q

Etomidate increases or decreases PONV

A

INCREASES

53
Q

Name a drug that can be very useful in anesthesia and sedation of high risk, pediatric, and asthmatic patients

A

ketamine

54
Q

pH and PKA of ketamine

A

pH 3.5-5.5

pka 7.5

55
Q

MOA of ketamine

A

antagonism of the NMDA receptors in the brain.

56
Q

antagonism of NMDA receptors on the brain results in…..

A

selective depressant effect on the medial thalamic nuclei that is responsible for blocking afferent signals of pain perception to the thalamus and cortex

57
Q

Where is the primary site of analgesic action of ketamine

A

thalamoneocortical system

58
Q

How does the NMDA receptor work?

A

NMDA receptor is a ligand-gated ion channel where Ca+ and Na+ are voltage dependent.

59
Q

Name the amino acid that is probably the most important excitatory neurotransmitter in the CNS

A

L-glutamate

60
Q

Is ketamine a competitive or noncompetitive antagonist at the NMDA receptor?

A

noncompetitive

61
Q

T or F Ketamine induced analgesia has a spinal cord component.

A

True

62
Q

describe the metabolism of ketamine

A

metabolism by the cytochrome P450 system is demethylation to form norketamine

63
Q

elimination of ketamine is primarily

A

renal

64
Q

T or F. The distribution kinetics of ketamine follows a two compartment model?

A

true

65
Q

The onset of a standard 2-2.5 mg/kg dose of ketamine has a faster or slower onset than propofol or etomidate

A

slower. 3-5 mins

66
Q

Why does ketamine have a slow elimination half life?

A

hepatic metabolism and excretion. A large amount of ketamine remains in the peripheral tissues as active drug and may be responsible for prolonged cumulative effects.

67
Q

what is the elimination half life of ketamine

A

2-3 hours

68
Q

Ketamine elimination is dependent or independent of hepatic blood flow?

A

dependent- the mean total body clearance is approximately the same as the hepatic blood flow

69
Q

Is distribution of ketamine dose dependent?

A

No (pg 114)

So that implies zero order kinetics????

70
Q

Which routes are available for ketamine administration? Which route has 93% bioavailability?

A

Oral
IM
IV

IM is 93% bioavailable

71
Q

Skeletal muscle tone increases or decreases with ketamine administration?

A

increases. muscle movements may occur unrelated to painful stimulus

72
Q

T or F. As with other IV induction agents, ketamine causes a decrease in CBF, CMRO2, and ICP

A

False, Increased

73
Q

Describe EEG changes you would expect when a pt loses consciousness as a result of Ketamine

A

transition from alpha to theta waves

74
Q

T or F Ketamine does not alter auditory evoked potentials

A

True

75
Q

Describe Ketamines effects on bp, hr, contractility, CO, CVP

A

all increased

76
Q

Injection of ketamine into the CNS causes an enhancement or inhibition of norepi uptake?

A

inhibits neuronal and extraneuronal uptake of norepi

77
Q

who may experience negative inotropic effects from ketamine?

A

critically ill with depleted catecholamine stores

78
Q

T or F- inhaled anesthetics may cause Ketamine to lower bp and CO

A

true- due to the decreasing sympathetic responses

79
Q

What ophthalmic changes are seen with ketamine?

A

increased IOP and nystagmus

80
Q

ketamine causes bronchodilation or constriction?

A

potent bronchodilator

81
Q

T or F. With ketamine administration central response to CO2 is maintained.

A

True

82
Q

Which antisalagogue is considered superior for administration with ketamine?

A

atropine (p116)

83
Q

ketamine is/is not highly lipid soluble…does/does not cross placenta?

A

IS highly lipid soluble and therefore does cross the placenta

84
Q

how do you use ketamine safely in obstetrics?

A

decreasing the dose to 0.2-1 mg/kg spares the neonate sedation issues

85
Q

ketamine may be the agent of choice in which peds populations?

A

difficult airway and reactive airway

86
Q

what structure is unique to midazolam vs other benzos

A

the imidazole ring

87
Q

T or F. midazolam is lipid soluble at pH less than 4.0

A

False, water soluble and does not require a lipoidal vehicle such as propylene glycol

88
Q

What happens to midaz in a physiologic pH greater than 4.0?

A

the diazepine ring closes and midaz becomes lipophilic which accounts for its rapid onset of action

89
Q

benzo MOA

A

agonist action at benzo receptor binding sites on the GABAa receptors throughout the CNS

90
Q

Of the three classes of ligands that bind to benzo receptors (agonists, antagonists, and inverse agonists)…midaz, diazepam, loraz would be considered ______?

A

agonists- increase binding affinity for GABA- resulting in opening of chloride channels, resulting in post synaptic membrane hyperpolarization- inhibiting neuronal transmission

91
Q

Give an example of a ligand that would be an antagonist at the benzo receptor

A

Flumazenil- forms a reversible bond with the agonist receptor but produces no agonist activity.

92
Q

Name an example of a long, intermediate, and short acting benzo

A

long diazepma
intermediate loraz
short midaz

93
Q

what is the T1/2 of midaz

A

less than 6 hours

94
Q

benzos are terminated by

A

redistribution out of the CNS

95
Q

of the 3 IV benzos…which is less dependent on hepatic cytochrome enzymes for metabolism? why?

A

lorazepam. it undergoes phase 2 conjugation to a significant extent. liver disease as well as hepatic enzyme induction or inhibition does not influence loraz as much as other drugs

96
Q

benzos- Volume of distribution- large or small?

protein binding- limited or extensive?

A

large

extensive

97
Q

which benzo may be useful in preventing chemo induced nausea and vomiting?

A

loraz

98
Q

benzos increase or decrease the threshold local anesthetic induced seizure activity

A

increase

99
Q

EEG changes associated with benzos

A

alpha disappears, beta activity is seen

100
Q

which benzo causes the most respiratory depression

A

midaz

101
Q

which patient population should avoid benzos

A

acute porphyrias

102
Q

flumazenil is a competitive or noncompetitive antagonist?

A

competitive

103
Q

onset and duration of flumazenil

A

1-2 mins, 45-90 mins

104
Q

flumazenil is contraindicated in whom?

A

pts with known history of seizures

pts who are benzo dependent and experience withdrawal

105
Q

MOA for precedex

A

selective alpha 2 agonist

106
Q

what accounts for the hypotensive side effects seen with precedeX

A

stimulation of imidazoline receptors

107
Q

when alpha 2 receptors are stimulated by an agonist what results?

A

decreased catecholamine release

108
Q

what is the main site of action for the sedative effects of precedex?

A

the pontine noradrenergic nucleus the locus coeruleus

109
Q

The alpha 2 receptors are what type of receptor?

A

G-protein coupled receptors

110
Q

When the G protein coupled receptors are activated….the result is activated or inhibited Ca+ channels, potassium channels?

A

inbibited Ca+, activated K, and direct modulation of exocytic release of proteins

111
Q

state the loading dose and infusion rate of precedex

A

1 mcg/kg over 10 mins, then 0.2-0.7 mcg/kg/HR

112
Q

T or F precedex is protein bound and undergoes almost complete biotransformation leaving very little unchanged in the urine and feces

A

True

113
Q

biotransformation of precedex involves….

A

direct glucuronidation

cytochrome P450-mediated metabolism

114
Q

Precedex causes increased, decreased, or unchanged CMRO2

A

unchanged

115
Q

Precedex is a drug of choice for what specific procedures?

A

procedures requiring a wake up test

116
Q

precedex does or does not interfere with electrophysiologic monitoring

A

does not. useful for brain mapping

117
Q

Effects of precedex on CBF

A

decreased due to vasoconstriction

118
Q

precedex analgesia and anesthetic effects work at what levels?

A

brain and spinal cord

119
Q

precedex enhances the analgesic effect of _______

A

N2O

120
Q

Main CV effects seen with precedex?

A

bradycardia and hypotension

121
Q

why does precedex cause hypoTN and bradycardia?

A

CNS alpha receptor stimulation and systemic vasodilation

122
Q

T or F- precedex does not interfere with neuro monitoring

A

true

123
Q

T or F: precedex is an alpha 2 agonist that results in central sympatholysis

A

TRUE

124
Q

Who should generic propofol be used in caution with?

A

Metabisulfite - allergy or asthma

Benzoyl alcohol - avoided in infants

Lindsays Flashcardlet (27 decks)

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