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Adv Pharm II > Final: adjunts, opioids > Flashcards

Final: adjunts, opioids Flashcards

1
Q

what is a medication that may be co administered with primary anesthetic to create a more balanced anesthesia

A

adjuvant

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2
Q

what are the non-opioid adjuvants

A

ofirmev
ketamine
toradol

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3
Q

what is the max dose of ofirmev

A

4g in 24hrs

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4
Q

what is a drug included in ofirmev solution

A

mannitol

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5
Q

what is the doses for ofirmev <> 50kg

A

<50kg= 15mg/kg
>50kg= 1000mg

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6
Q

what are contraindications for ofirmev

A

liver impairment
mannitol allergy

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7
Q

what is an advantage of ofirmev over toradol

A

does not increase bleeding time

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8
Q

what are some se of ofirmev

A

vomit
headache
insomnia

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9
Q

is ketamine competitive or non competitive

A

non competitive

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10
Q

what is the moa of ketamine

A

inhibits nmda receptor

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11
Q

what part of brain does ketamine inhibit impulses to, which causes dissociation

A

limbic cortex

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12
Q

what is the only primary anesthetic that also provides analgesia

A

ketamine

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13
Q

ketamine has a ________________ effect with volatiles

A

synergistic

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14
Q

ketamine has an ___________________ effect with propofol/benzos

A

additive

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15
Q

which is a larger effect, additive or synergistic effect

A

synergistic

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16
Q

what is the dose of ketamine

A

iv: 1-2 mg/kg
im 4-8 mg/kg

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17
Q

what is the onset, peak, doa of ketamine

A

30 s, 1 min, 5-15 min

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18
Q

what is the half life of ketamine

A

2-3 hour

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19
Q

how is ketamine metabolized

A

redistribution

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20
Q

what are the se of ketamine

A

hallucinations
increased salivation
nystagmus

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21
Q

how can you decrease hallucinations/salivation with ketamine

A

versed/robinol

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22
Q

what conditions would you want to avoid giving toradol

A

asthma
nasal polyps
rhinitis
hypovolemia

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23
Q

how is toradol eliminated

A

kidneys

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24
Q

what drug works by inhibit prostaglandin synthesis

A

toradol

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25
Q

what is the peak, onset, doa of toradol

A

10 min, 1 hour, 4 hour

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26
Q

ponv occurs in what % of general surgery

A

30%

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27
Q

what are some risk factors of ponv

A

female
hx of ponv
non smoker
young age
volatiles
post op opioids
duration of anesthesia
surgery type
general vs regional

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28
Q

what are sx of anticholinergic syndrome

A

restlessness
hallucinations
somnolence
unconsciousness

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29
Q

which anti-emetic can cause anti cholinergic syndrome

A

scopolamine

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30
Q

what is the dose of scopolamine

A

1.5mg patch transdermal
place at least 4 hours before surgery
remove after 24 hours
do not touch eyes- mydriasis

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31
Q

what is zofran drug class

A

5 ht3 antagonist

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32
Q

what is dose of zofran

A

adult: 4mg pre emergence
ped: 0.15mg/kg

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33
Q

what is onset/peak/doa of zofran

A

30 min, 2 hr, 4-24 hr

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34
Q

what is the bb warning for zofran

A

qt prolongation

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35
Q

what are sx of anticholinergic od

A

blurred vision
dry/flushed skin
rash on feac/neck chest
dry mouth
bowel/bladder loses tone
tachycardia

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36
Q

what kind of patient should you monitor ecg when giving zofran

A

electrolyte imbalance
chf
taking other qt prolonging drugs

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37
Q

when is decadron given

A

prior to induction

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38
Q

what common operative med should be cautioned in diabetics

A

decadron- increases glucose

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39
Q

what is reglan usually given in combination with

A

pepcid

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40
Q

what are se of reglan

A

extrapyramidal sx: involuntary muscle contraction, tremor, rigid muscle, tardive dyskinesia

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41
Q

when is reglan indicated

A

gerd
gastroparesis
full stomach prior to emergency case

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42
Q

what drug enhance ach transmission on intestinal smooth muscle, which increases lower esophageal sphincter tone, speeding up gastric emptying

A

reglan

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43
Q

what antiemtic can cause perineal burning

A

decadron

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44
Q

what are the h1 receptor antagoinsts

A

benadryl
promethazine
dimenhydrinate

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45
Q

t or f- benadryl alone causes decreased ventilatory drive

A

false

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46
Q

what drug is often combined with opioids to potentiate analgesia

A

promethazine

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47
Q

what drug must be metabolized in diphenhydramine to be effective

A

dimenhydrinate

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48
Q

why does promethaine have a low bioavailability

A

extensive 1st pass effect in live

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49
Q

what alpha 2 agonist has local anesthetic effects on peripheral nerves

A

clonidine

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50
Q

what med is added to local anesthetic solutions to increase doa

A

clonidine

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51
Q

what drug decreases sns activity by reducing circulating catecholamines

A

clonidine

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52
Q

what are some se of clonidine

A

dizzy
bradycardia
dry mouth
do not abruptly stop

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53
Q

what is epidural dosing of clonidine

A

30mcg/hr in mixture of opioid or local

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54
Q

what types of analgesia does precedex supply

A

supraspinal and spinal

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55
Q

what are some se of precedex

A

decreased salivation
bradycardia
decreased shivering
variable htn/hotn

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56
Q

what is a main advantage of precedex

A

preserves resp drive

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57
Q

where is precedex mainly metabolized

A

liver

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58
Q

what is preferred for awake fiberoptic intubation: precedex or ketamine

A

precedex

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59
Q

what is the alpha 2 agonist class of precedex

A

imidazoline

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60
Q

what is the site of action of precedex

A

locus coeruleus

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61
Q

what are some of the moa of precedex specifically

A

decreases catecholamine releasing–>
inhibit ca and k channel activation–>
hyperpolarizes cell

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62
Q

push precedex as fast as possible for best effect

A

no- may cause hypertension because sns effect will occur before cns effects are able to kick in and overpower sns effects

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63
Q

what is the moa of benzos

A

gaba agonist

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64
Q

how is versed metabolized

A

cyp450

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65
Q

what are the 3 positive effects of versed

A

amnesia
sedation
anxiolysis

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66
Q

what drugs does versed have a synergistic effect with

A

prop and fent

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67
Q

what channel do gaba receptors effect and how

A

chloride- opens channels leading to hyperpolarization

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68
Q

what is a dopamine receptor blocker antipsychotic

A

droperidol

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69
Q

what disease would you want to avoid droperidol

A

parkinsons

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70
Q

how can droperidol effect ekg

A

prolong qtc

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71
Q

t or f- droperidol causes sedation and anti-emetic effects

A

true

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72
Q

what is a risk of droperidol admin

A

extrapyramidal effects
neuroleptic malignant syndrome

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73
Q

what receptors do opioids work on

A

mu, delta, kappa

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74
Q

what side effects will adjuvant opioids help decrease with volatile

A

myocardial depression

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75
Q

t or f- opioids causes spinal analgesia only

A

f- supraspinal and spinal

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76
Q

what can opioids do to muscles

A

muscle rigidity

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77
Q

what are the mu receptor prototypes

A

morphine
fent

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78
Q

what are the delta receptors prototypes

A

deltorphin

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79
Q

what are the kappa receptors prototypes

A

buprenoprhine
pentazocine

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80
Q

which opioid receptor does not cause resp depression/gi effects/sedation

A

delta

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81
Q

what receptor has endogenous ligands of beta endorphine, endomorphin

A

mu

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82
Q

what receptor has endogenous ligands leu/met enkephalin

A

delta

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83
Q

what receptor has endogenous ligands dynorphin

A

kappa

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84
Q

desflurane can be reduced by 85% by administering what

A

fent 1.5 mcg/kg 5 mins before incision

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85
Q

t or f- remifentanil is metabolized by liver

A

false
esterases

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86
Q

what opioid is best for rapid recovery

A

remifentanil
5-10 min DOA

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87
Q

what is the MOA of reglan

A

enhances ACH transmission on intestinal smooth muscle thereby increasing lower esophageal sphincter tone, speeding up gastric emptying, and lowering gastric fluid volume

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88
Q

what is the dose for reglan

A

10 mg IV 15-30 min prior to induction (push over 5 min)

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89
Q

what are SE of reglan

A

extrapyramidal symptoms (involuntary muscle contractions, tremors, rigid muscles, tardive dyskinesia)

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90
Q

what are the side effects of Decadron

A

increases BS
delays wound healing
perineal burning

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91
Q

what is the dose of diphenhydramine

A

25-50 mg (0.5-1.5 mg/kg) oral, IM, IV q3-6 hrs

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92
Q

what is the MOA of promethazine

A

antihistamine, antimuscarinic

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93
Q

what is the dose of promethazine

A

12.5-50 mg q4-12 hrs

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94
Q

what is a prodrug of diphenhydramine

A

Dimenhydrinate

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95
Q

What is the MOA of alpha 2 agonists?

A

Inhibit NE release, reducing sympathetic outflow

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96
Q

what are the effects of Clonidine

A

decreased sympathetic activity, enhance parasympathetic tone, reduced circulating catecholamine

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97
Q

what are epidural/caudal/PNB effects of Clonidine

A

adjunct for anesthesia and analgesia
treats chronic neuropathy pain to increase efficacy, Segmental

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98
Q

what are the side effects of Clonidine

A

sedation, dizziness, bradycardia, dry mouth

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99
Q

what can abruptly stopping clonidine lead to

A

rebound htn
agitation
sympathetic overactivity

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100
Q

what is dosing of clonidine

A

30 mcg/hr in mixture with opioid or local

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101
Q

what is MOA of precedex

A

G-Protein-Coupled receptors on presynaptic nerve endings
Inhibit the activation of Ca++ and K+ channels, thus hyperpolarizing the cell

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102
Q

what is the site of action of precedex

A

Pontine and locus coeruleus

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103
Q

what are some side effects of precedex

A

transient htn
minimal effects of resp drive

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104
Q

precedex effects picture

A
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105
Q

what is the 1/2 life of precedex

A

6-8min

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106
Q

how is precedex metabolized

A

liver

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107
Q

what does versed work synergistically with

A

propofol and opioids

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108
Q

what kind of drug is droperidol

A

antipsychotic

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109
Q

what is the blackbox warning on droperidol

A

prolong QTc

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110
Q

what are risks of Droperidol

A

> QTC
extrapyramidal effects
neuroleptic malignant syndrome

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111
Q

opioids effect picture

A
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112
Q

which opioid receptor causes resp depression, GI effects, and sedation

A

mu

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113
Q

opioid receptor chart

A
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114
Q

what is the parent compound for many sympathomimetics

A

B-phenylethlamine

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115
Q

what is a 3,4-hydroxyl substitution of B-phenylethylamine

A

dopamine

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116
Q

what is the metabolic precursor for norepinephrine and epinephrine

A

dopamine

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117
Q

what decreases the activity of norepi at B-receptors

A

lack of an N-substitution in the B-phenylethylamine

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118
Q

what classes of medications increase Ca++ interaction with cardiac actin and myosin

A

B-agonists
phosphodiesterase inhibitors
cardiac glycosides

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119
Q

what medications act on the B-1 receptor

A

epinephrine
dobutamine
dopamine
isoproterenol
to a lesser extent
-ephedrine
-norepinephrine

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120
Q

what the is physo of B1 activation

A

acts on cardiac myocyte sarcolemma
activates G3 protein
activates adenylyl cylclase
increased cyclic AMP
activates protein kinase A
increased opening of voltage gated Ca++ channels

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121
Q

What is the MOA of phosphodiesterase inhibitors?

A

inhibits breakdown of cAMP by inhibiting PDE3,

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122
Q

what kind of drug is milrinone

A

phosphodiesterase inhibitor

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123
Q

what vasopressor acts on the V1 receptor to cause vasoconstriction

A

vasopressin

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124
Q

what drugs are in the catecholamine class of drugs

A

epi
norepi
dopamine
dobutamine
isoproterenol

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125
Q

t/f phenylephrine is a catecholamine

A

false

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126
Q

what sympathomimetic are excreted unchanged in the urine

A

ephedrine, milrinone

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127
Q

what metabolizes vasopressin

A

vasopressinases in the liver and kidney

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128
Q

what metabolizes most cathecholamines

A

COMT (catechol-o-methyltransferase)
MAO (monoamine oxidase)

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129
Q

which catecholamine is not metablized by MAO

A

dobutamine

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130
Q

where are alpha-1 receptors located

A

peripheral vasculature (vasc smooth muscle)

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131
Q

what do B1 receptors modulate

A

inotropy
chronotropy
lusitropy

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132
Q

where are B2 receptors located? what do they stimulate

A

-widely distributed in vasculature
-dilation of muscular, splanchnic, renal vasculature
-Bronchodilation

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133
Q

what is lusitropy

A

ventricles to relax

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134
Q

what receptors does dobutamine work on

A

B1 B2

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135
Q

what is the drug of choice septic shock with systolic dysfunction

A

dopamine

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136
Q

what is the drug of choice for stress echocardiography

A

dobutamine

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137
Q

what is the drug of choice for weaning from cardiopulmonary bypass

A

milrinone

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138
Q

what is the drug of choice for post-cardiopulmonary bypass vasoplegia

A

vasopressin

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139
Q

what cell synthesizes, stores, and releases epinephrine

A

chromaffin in adrenal medulla

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140
Q

how does epi effect mucosal edema

A

decreases

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141
Q

how does epi effect mast cells

A

stabilizes so decreased histamine, tryptase, other inflammatory mediators

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142
Q

how does epi effect CPP during codes

A

increased

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143
Q

what is the number one factor that increases myocardial oxygen consumption

A

HR

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144
Q

what medication do you give to treat hypotension with a decrease in HR and/or low cardiac output

A

EPI

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145
Q

what receptor does epi stimulate to cause bronchodilation and mast cell stabilization

A

B2

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146
Q

how does epi effect BS

A

hyperglycemia from
-increased liver glycogenolysis
-reduced uptake of glucose
-inhibits release of insulin

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147
Q

what are some adverse effects of epi

A

hyperglycemia
hypokalemia
lactic acidosis
myocardial ischemia

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148
Q

what can happen if you give epi to a patient with acute cocaine intoxication

A

Myocardial ischemia
stroke

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149
Q

what conditions is epi contraindicated in

A

cocaine intoxication
tetraology of fallot
hypertrophic obstructive cardiomyopathy
digitalis
halothane
BBs

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150
Q

what is the primary neurotransmitter of the sympathetic NS

A

norepi

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151
Q

where is norepi released from

A

postganglionic nerve endings

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152
Q

what are adverse effects of norepi

A

-severe HTN causes increased cardiac workload and cardiac ischemia
-organ dysfunction from lack of blood flow

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153
Q

where are D1 receptors located

A

mesenteric and renal vasculature

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154
Q

what two affects does dopamine have on renal function

A

diuresis
naturesis

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155
Q

when in low concentrations, what is the action of dopamine

A

D1 (renal, mesenteric, coronary vasc) vasodilation
increased GFR and renal blood flow
increased Na excretion and urine output
decrease SVR

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156
Q

what do high doses of dopamine do

A

directly stimulate B1 receptors
enhance release of norepi
increased contractility
increased HR
increases BP
alpha-1 vasoconstriction

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157
Q

what are adverse effects of dopamine

A

tachycardia
tachyarrhythmias
myocardial ischemia
decreased splachnic perfusion
gut ischemia
reduced ventilatory response
hypoxemia
decreased GH, prolactin, TSH

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158
Q

what kind of medication is dobutamine

A

direct-acting synthetic catecholamine

159
Q

how does dobutamine effect cardiac filling pressures and PVR

A

decreases

160
Q

what are adverse effects of dobutamine

A

tachy
arrhythmias
hypertension
exacerbate MI

161
Q

what are end effects of milrinone

A

increases CI
reduces art pressure
reduces LVEDP
reduces PVR

162
Q

why is milrinone effective in treatment of RHF

A

increases vent contractility
decreasing PVR

163
Q

what is a possible issue with milrinone and RHF

A

decreases SVR, so combine with norepi or vasopressin

164
Q

how does phenylephrine effect lungs

A

pulmonary vasoconstriction and pulmonary htn

165
Q

what are adverse effects of phenylephrine

A

severe brady
brief asystole
reduced CO
pulme edema
arrhythmias
cardiac arrest

166
Q

what do you give if phenylephrine causes severe hypertension

A

phentolamine (alpha-1 antagonist)
hydralazine (direct arterial dilator)

167
Q

T/F BB and CCB are effective ways to treat htn caused by phenylephrine

A

F, can cause cardiac depression and acute heart failure

168
Q

where is vasopressin stored and released from

A

posterior pituitary gland

169
Q

what effects the hemodynamic effects of vasopressin

A

presence/absence of sympathetic and renin-angiotensin systems

170
Q

what are adverse effects of vasopressin

A

reduced mucosal perfusion
increases liver enzymes
total bilirubin concentrations
decreases platelet count

171
Q

what is the physo effects of ephedrine

A

increase in systolic, diastolic, and MAPA
increased myocardial contractility
increases HR
increases CO

172
Q

T/F ephedrine can cross the BBB

A

T, causes agitation and insomnia

173
Q

what happens is a patient taking MAOIs take ephedrine

A

exaggerated hypertensive effect

174
Q

what is the main center for neurogenic control of vascular tone

A

vasomotor center in midbrain

175
Q

what are the two central neural systems that regulate bp

A

neurogenic control
baroreceptor reflexes

176
Q

what are other humerol/endocrine control of BP

A

RAAS, ANP, renal Na/H2O secretion, eicosanoids, kallikrein-kinin system, adrenal steroids, endothelin system, medullipin

177
Q

what are the three ways that drugs can treat high BP

A

1) effect ANS
2) inhibit RAAS
3) peripheral vasodilation

178
Q

what are examples of arterial vasodilators

A

prazosin
phentolamine
phenoxybenzamine
tolazoline
hydralazine
diazoxide
CCBs
ACE inhibitors

179
Q

what are examples of veno/arteriolar dilators

A

nitroprusside

180
Q

what are examples of venodilators

A

nitroglycerine

181
Q

name the alpha 1 blockers

A

doxazosin, prazosin, indoramin

182
Q

name the a1,a2 blockers

A

phentolamine, phenoxybenzamine

183
Q

what are the a1, b1 blockers

A

labetalol, carvedilol, nebivolol

184
Q

what are examples of nitrovasodilators

A

nitric oxide
sodium nitroprusside
nitroglycerine
isosorbide dinitrate
isosorbide mononitrate

185
Q

what is the MOA of CCBs

A

arterial vasodilation by blockade of Ca++ influx through L-type voltage gated Ca++ channels
may also reduce HR (chronotropy)
and contractility (inotropy)

186
Q

what are the three types of CCBs

A

dihydropyridine
phenylalklamine
benzothiazepines

187
Q

what are examples of dihydropyridines

A

nifedipine, nicardipine

188
Q

what is site of action of dihydropyridines

A

resistance vessels with minimal effects on veins

189
Q

what is the site of action of phenylalklamines

A

heart

190
Q

what is the effect of CCBs on the heart

A

reduce HR and contractility thus decreasing CO and BP
(negative chronotropy and inotropy)

191
Q

what is the site of action of benzothiazepines

A

vasculature

think diltiazem

192
Q

how do B1 and B2 receptors have action

A

increase Camp

193
Q

what does activation of B3 lead to

A

cardiodepression

194
Q

what are the b1 selective blockers

A

acebutolol
atenolol
bisopropol
celiprolol
esmolol
xamoterol

195
Q

what are the partial inverse agonists

A

metoprolol
nebicolol

196
Q

how do BBs decrease BP

A

decreasing CO (by decreasing contractility and HR)
inhibiting the release of renin from the kidneys

197
Q

what are the nonselective BBs

A

propranolol
timolol
Nadolol
Sotalol

198
Q

what are the pharm effects of alpha-2 receptor agonists

A

sedation, analgesia, hypotension

199
Q

what is the result of alpha-2 binding

A

decreased cAMP
hyperpolarization
decreased intracellular Ca++

200
Q

How do alpha 1 antagonists work?

A

block receptor to prevent Ca++, causing smooth muscle relaxation AKA vasodilation

201
Q

how does NO effect renal system

A

renal vasodilation= diuresis and natriuresis

202
Q

what NO vasodilator releases NO spontaneously

A

sodium nitroprusside

203
Q

what NO vasodilator need active reduction to have effect

A

organic nitrates like nitroglycerin

204
Q

what kind of toxicity does sodium nitroprusside cause

A

cyanide

205
Q

does nitroglycerin do more venous or arterial dilation

A

venous

206
Q

what are the cardiac effects of nitroglycerin

A

decreased BP
reduced preload
reduced myocardial oxygen demand
coronary vasodilator

207
Q

what phase of the AP does adenosine effect

A

phase one, calcium entry

208
Q

what are the action of adenosine

A

stimulate NO=coronary vasodilation
activate K channels= hyperpolarize
blocks Ca entry= vascular relaxation

209
Q

what is the MOA of hydralazine

A

promotes influx of K into vascular smooth muscle= hyperpolarize= muscle relaxation
-may inhibit Ca release from SR

210
Q

What is dromotropy?

A

conduction velocity of AV node

211
Q

what is the chemical structure of diltiazem

A

benzothiazepine

212
Q

how does aging effect CCBs

A

reduced cardiac output leads to increased bioavailability and decreased clearance

213
Q

what receptors does carvedilol block

A

Alpha 1, Beta 1, Beta 2

214
Q

what are negative effects of BB

A

-negative inotropy
-worsened intermittent claudication, raynauds in patient with peripheral vasc disease
-bradycardia=synchopy
-nonselectives can cause bronchospasm and worsen asthma
-increased triglycerides
-lipophilic BBs can cause CNS depression, sleep disturbances, vivid dreams, and hallucinations
-sudden withdrawal can cause reflex tachy, htn, and palpatiation

215
Q

how do BBs effect insulin

A

potentiate effects of insulin and other oral hypoglycemic agents

216
Q

what kind of antiarrhhythmic is lidocaine

A

1b, sodium channel blocker

217
Q

what kind of antiarrhhythmic is verapamil and clevidipine

A

4, CCB

218
Q

what kind of antiarrhythmic is amiodarone

A

class 3, potassium channel blocker

219
Q

what kind of antiarrhythmic is metoprolol, esmolol, labetalol

A

class 2, beta blocker

220
Q

how do class 3 antiarrythmics effect EKG

A

QT prolongation

221
Q

when do you not use BBS

A

diabetes-masks symptoms of hypoglycemia
tachycardia from phenylephrine
HF
asthma- if non selective
peripheral vasc disease- if non selective

222
Q

what are the heart effects of CCBs

A

negative inotropy
negative chronotropy
negative dromotrope

223
Q

all local anesthetics are weak __________

A

bases

224
Q

3what are molecular components of all local anesthetics

A

aromatic ring
intermediate ester or amide link chain
tertiary amine end

225
Q

the aromatic ring makes LA ________philic

A

lipo

226
Q

what would make LAs hydrophilic

A

when there is an excess positive charge (protonated)

227
Q

what LAs are in the Ester family

A

cocaine
procaine
2-chloroprocaine
tetracaine

228
Q

what metabolizes most esters except cocaine

A

plasma cholinesterase

229
Q

what metabolizes cocaine

A

liver (hepatic carboxylesterase)

230
Q

which patients have an increased risk for LAST from ester LAs

A

plasma cholinesterase deficiency

231
Q

what conditions decrease plasma cholinesterase

A

hepatic impairment
increased BUN
chemotherapeutic drugs
expectant mothers

232
Q

which kind of LA has more allergic reactions

A

esters

233
Q

how are amides metabolized

A

liver cyp450

234
Q

which amide is not metabolized by CYP450

A

articaine, plasma carboxyesterase

235
Q

agents with lower pKa are more ______________ at physiologic ph (7.4)

A

non ionized

236
Q

which form of drug penetrates the lipid bilayer and has effect

A

nonionized

237
Q

low pKa means (slower/faster) onset

A

faster

238
Q

what is goal channel that LAs block

A

Na channels

239
Q

what is definition of pKa

A

The pH at which the molecule is 50% ionized and 50% nonionized

240
Q

why do LAs not work in infected, acidotic tissues

A

these tissues have a pH of 6, which means most of the LA is ionized

241
Q

what can we add to LA to increase speed of onset

A

bicarb, because it is more basic, this brings the tissue pH closer to the LA pKa

242
Q

what is the pKa of procaine

A

8.9

243
Q

what is the pKa of tetracaine

A

8.6

244
Q

what is the pKa of bupivicaine

A

8.1

245
Q

what is the pKa of Ropivicaine

A

8.1

246
Q

what is the pKa of Chloroprocaine

A

8.7

247
Q

what is the pKa of Lidocaine

A

7.7

248
Q

what is the pKa of Etidocaine

A

7.7

249
Q

what is the pKa of Mepivicaine

A

7.6

250
Q

increased lipid solubility correlates with _____________ penetration of the nueral membrane by local anesthetic

A

increased

251
Q

what determines the potency of LAs

A

lipid solubility AKA oil:water partition coefficient

252
Q

what molecular structure determines the lipophilicity of LAs

A

alkyl substituents on the aromatic ring and on or near the tertiary amine

253
Q

the larger the alkly substituent of the LA the _____ the lipophilicity AKA potency

A

higher

254
Q

a higher lipid solubility of LA increases what two aspect of pharmokinetic and decreases what aspect

A

potency
DOA
decreases onset

255
Q

what are the two determinates of DOA of LA

A

protein binding and lipid solubility

256
Q

the greater the protein binding the __________ the DOA

A

longer

257
Q

what can we give with LAs to increase DOA

A

epi (vasoconstriction)

258
Q

what are the four determininants of blood concentrations of LAs

A

-presence of a vasoconstrictor
-tissue blood flow
-concentration injected
-number and frequency of injection

259
Q

what causes most of LA to be lost from injection site

A

vascular absorption

260
Q

a site of LA injection with high rates of vascular uptake is (more/less) likely to have LAST

A

more

261
Q

rank high to low vascular uptake sites for LA

A

IV
tracheal
intercostal
caudal
paracervical
epidural
brachial plexus
subarachnoid, sciatic, femoral
subcutaneous

262
Q

the higher the concentration of LA at site, the _______ the conduction block

A

longer

263
Q

the lower the blood flow to site of LA injection site the _______ the conduction block

A

longer

264
Q

what areas do we not add epi to LA

A

lacking collateral vessels (terminal circulation)
fingers
nose
toes
ear

265
Q

what is a steroidal adjuvent to prolong LA block

A

dexamethasone

266
Q

what alpha-2 agonist can we add to increase duration of both motor and sensory blocks

A

precedex

267
Q

what alpha-2 agonist cab be added to epidural and intrathecal to produce more analgesic effects

A

clonidine

268
Q

what opioid can prolong action of LA

A

ketamine

269
Q

what analgesic adjuvent can be given to increase the duration of SAB

A

mg

270
Q

what drug can be given with LA to speed onset

A

sodium bicarb

271
Q

what benzo can be given with LA to increase DOA of SAB

A

versed

272
Q

LA prevent _________ influx into the nerve axon

A

Na

273
Q

what electric process do LA inhibit

A

action potential

274
Q

what state of the sodium channels to LA bind with

A

open and inactivated more than the resting

275
Q

what type of nerve fibers do LA bind with most easily

A

faster conduction velocities such as small myelinated A-gamma motor and A-delta sensory
then A-alpha and A-beta
then the small nonmyelinated C fibers

276
Q

why do LA bind to nerves with faster conduction velocities

A

1) more binding sites are available during activated states
2) LA binding last longer on previously inactivated sites than on resting sites

277
Q

what is it called when LA in epidural/spinal cuase autonomic blockade but not sensory/motor blockade

A

differential blockade

278
Q

how much higher is sympathetic blockade then motor/sensory blockade in neuraxial block

A

6 dermatomes

279
Q

how many nodes of ranvier must be blocked in a myelinated nerve to stop nerve conduction

A

2-3 nodes

280
Q

the greater the frequency of APs the ________ the onset of the LA block

A

faster

281
Q

where are voltage gated sodium channels found

A

only in axon

282
Q

what LA concentrations are decreased when it passes through pulmonary circuit

A

lidocaine
bupivicaine
priolocaine

283
Q

what metabolizes ester LA

A

plasma psuedocholinesterase

284
Q

what metabolizes amide LA

A

cyp450

285
Q

what population has a prolonged elimination of amides

A

neonates and infants

286
Q

what causes the neonatal toxicity from lidocaine

A

accumulation of its major metabolite, monoethylglycineexylidide

287
Q

what two diseases cause a exteneded half life clearance of lidocaine

A

CHF
liver disease

288
Q

what is the goal of liposomal LA

A

increase amount of LA in the liposome and have a consistent release of LA into tissues

289
Q

what LA can be incorporated into liposomes

A

Lidocaine
tetracaine
bupivacaine

290
Q

what is the max dose of bupivacaine
mg:
mg/kg:

A

175 mg
2 mg/kg (2.5 mg/kg with epi)

291
Q

what is the max dose of ropivacaine
mg:
mg/kg:

A

200 mg
3 mg/kg

292
Q

what is the max dose of lidocaine
mg:
mg/kg

A

300 mg
4.5 mg/kg (7 with epi)

293
Q

what is the max dose of mepivacaine
mg:
mg/kg:

A

300 mg
7 mg/kg

294
Q

what is the max dose of prilocaine
mg:
mg/kg:

A

400 mg
6 mg/kg

295
Q

increased dose ________ doa while ________ time of onset

A

increases
decreases

296
Q

T/F when you reach the max dose of lidocaine, you can then switch an use prilocaine

A

F, they are additive

297
Q

what is ED95

A

effective dose in 95% of patients

298
Q

what are the two onset of last

A

immediate
delayed 2/2 redistribution/absorption from highly vascular tissues

299
Q

which occurs first, CNS or cardiovascular signs of last

A

CNS

300
Q

what is the initial CNS patho of LAST

A

-blockade of inhibitory pathways in the cerebral cortex
-unopposed release of the excitatory neurotransmitter glutamate
OR
suppression of both inhibitory and excitatory circuits leading to profound CNS depression

301
Q

how does CNS depression from LAST effect lungs

A

resp depression leads to resp acidosis, elevated CO2 causes cerebral vasodilation, which delivers more LA to brain, then resp failure (this is a positive feedback loop)

302
Q

how does elevated CO2 levels in LAST prolong LAST effects

A

CO2 enters cells, causing acidosis, more LA is in ionized form which cannot exit the cell, this leads to ion trapping of LA intracellularly and further CNS effects

303
Q

how does increased CO2 effect LA protein binding

A

plasma protein binding of LA is decreased, leading to higher concentrations of unbound and further CNS toxicity

304
Q

how do you avoid all the issues caused by resp depression/acidosis in LAST

A

adequately ventilate patient,

305
Q

what three ways does LAST effect cardiovascular pathophysiology

A

directly
sympathetic blockade
parasympathetic blockade

306
Q

what causes the profound hypotension in last

A

relaxation of vascular smooth muscle in the arterial tree

307
Q

how does LAST effect EKG

A

lengthened PR interval
lengthened QRS complex

308
Q

how does LAST effect ventricular function

A

slows rate of depolarization of purkinje fibers and ventricular muscle by blocking fast Na channels

309
Q

what rhythms occur in LAST

A

bradycardia
cardiac arrest
2/2 dampened pacemaker activity in the sinus node

310
Q

how does LAST effect contractility

A

negative inotropy
inhibits Ca++ from SR
inhibits Na and Ca currents

311
Q

what three lab values increase the negative inotropic and chronotropic effects while increasing arrhythmias in LAST

A

hypercapnia
acidosis
hypoxia

312
Q

what three medications decrease the threshold for cardiac toxicity in LAST

A

BBs
CCBs
Digoxin

313
Q

what is treatment for LAST

A

Airway-intubate
Breathing-Ventilate
Circulation
Drugs:
intralipid (lipid emulsion)
benzodiazipines: for seizures
muscle relaxants to secure airway
cardiovascular support/resuscitation

314
Q

what medications do we avoid in LAST

A

vasopressin
CCBs
BBs
LAs
reduce epi doses to 1 mcg/kg

315
Q

what is method for lipid emulsion for LAST

A

1.5 ml/kg bolus then continuous infusion of 0.25 ml/kg/min
IF STILL UNSTABLE
another bolus then infusion of 0.5 ml/kg/min

316
Q

how can we prevent LAST

A

-gentle aspiration
-aspirate frequently(every 5ml) /continuous
- monitor EKG for QRS changes

317
Q

what happens with a lidocaine plasma concentration of 1-5 mcg/ml

A

analgesia

318
Q

what happens with a lidocaine plasma concentration of 5-10 mcg/ml

A

light-headedness
tinnitus
visual disturbances
numbness of tongue
muscle twitching
seizures
convulsions

319
Q

what happens with a lidocaine plasma concentration of 10-15 mcg/ml

A

seizures/convulsions

320
Q

what happens with a lidocaine plasma concentration of 15-25 mcg/ml

A

unconsciousness
coma
resp arrest

321
Q

what happens with a lidocaine plasma concentration of >25 mcg/ml

A

cardiovascular suppression

322
Q

what are early CNS s/s LAST

A

dizziness, lightheadedness, facial n/t, auditory/visual disturbances, ringing in ears, slurred speech, drowsiness, disorientation

323
Q

what are progressive CNS s/s LAST

A

tremors, twitching, shivering, tonic-clonic sz,

324
Q

what are late CNS s/s LAST

A

sz activity stops
resp arrest

325
Q

what are CV s/s LAST

A

hypotension
bradycardia
tachycardia
arrhythmias (Vtach, Vfib)
arrest

326
Q

how does prolonged use of edrophonium, physostigmine and echothiophate effect LA

A

depressed psuedocholinesterase leasts to prolonged ester LA activity

327
Q

what kind of LA has PABA (para-aminobenzoic acid) as a metabolite

A

esters

328
Q

how does cocaine differ from other ester LAs

A

its a vasoconstricor
its naturally occuring

329
Q

T/F ester LAs accumulate in the blood

A

F, they are metabolized by plasma psuedocholinesterase

330
Q

what LA is good for pregnant patient

A

chloroprocaine (fast metabolism)

331
Q

which ester LA is most likely to have LAST

A

tetracaine

332
Q

what LA is used to assess plasma cholinesterase activity

A

dibucaine (high incidence of LAST)

333
Q

what is normal dibucaine result

A

70-85% depression or 80%

334
Q

what dibucaine number means homozygote atypical pseudocholinesterase

A

20

335
Q

what dibucaine number is heterozygotic atypical pseduocholinesterase

A

30-70

336
Q

what LAs are effected by atypical psuedocholinesterase

A

esters

337
Q

what LA can cause methemoglobinemia

A

prilocaine, bupivicaine

338
Q

what is treatment for methemoglobinemia

A

methylene blue

339
Q

ester local anesthetics are derivatives of ________

A

benzoic acid

340
Q

what causes bradycardia in subarachnoid injection

A

blockade of cardiac sympathetic preganglionic fibers, which arise from segments T1-T4

341
Q

compared to sensory blockade, motor blockade occurs _______ segments lower

A

2-3

342
Q

compared to sensory blockade, sympathetic blockade occurs __________ segments higher

A

2-6

343
Q

your patient becomes nauseous 5 minutes after a spinal anesthetic, what is likely the cause

A

hypotension

344
Q

how much do you reduce LA admin in parturient epidural

A

25-50%

345
Q

what causes the hypotension associated with spinal and epidural anesthesia

A

blockage of sympathetic preganglionic nerves

346
Q

what is an immune system response to a foreign, environmental antigen that causes an altered T cell and antibody response

A

hypersensitivity

347
Q

what is the time frame for. a type 1 hypersensitivity reaction

A

15-30min

348
Q

what antibodies act in type 1 hypersensitivity

A

IgE

349
Q

where do IgE antibodies bind to in type 1 hypersensitivity

A

mast cells and basophils

350
Q

what does a second exposure to the antigen do in type 1 hypersensitivity

A

-cross linking of two IgE antibodies on mast cells and basophils
-increased Ca++ inflyx
-Ca++ degranulates mast cells releasing mediators

351
Q

what mediators are released from mast cell degranulation in type 1 hypersensitivity

A

-histamine
-heparin
-proteolytic enzyme
-chemotactic factors

352
Q

what other mediators are activated by mast cell degranulation in type 1 hypersensitivity

A

bradykinin, leukotrienes, interleukins, serotoinin, prostaglandins, thromboxane

353
Q

what is the most important mediator of type 1 hypersensitivity reaction

A

histamine

354
Q

what results from binding of Histamine to H1 receptors in type 1 hypersensitivity

A

bronchoconstriction, increased vasc permeability, vasodilation, urticaria, pruritis, increased gut permeability, increased mucus

355
Q

T/F type one hypersensitivity happens on first exposeure

A

F, happens on second

356
Q

what can a severe allergic reaction lead to

A

angioedema
systemic vasodilation
hypotension
extravasation of protein and fluid
bronchospasm
dysrhythmias

357
Q

how fast does anaphylaxis occur

A

within min

358
Q

how do we treat type 1 hypersensitivity reaction

A

-antihistamine (benadryl)
-cromolyn sodium (inhibit mast cell)
-bronchodilators like B2 agonists (albuterol)
-leukotriene receptor blocker (singulair)
-inhibitors of cyclooxygenase pathways (zileutoin)

359
Q

how do you diagnose a type 1 hypersensitivity individual

A

skin tests with allergen
immunoassays to measure IgE
tryptase

360
Q

what medications can cause intraop anaphylasxis

A

anesthetics, antibiotics, antiseptics, blood products

361
Q

what are the most frequent cause of anaphylactic reactions intraop

A

NMBA
1-succs
2-vec
3-atracurium
4-pancuronium
5-mivacurium
6-cisatracurium

362
Q

what molecular strucutres cause anaphylactic reaciton is NMBs

A

quatinary ammoniums

363
Q

what are the second and third leading causes of anaphylaxis intraop

A

abx
latex

364
Q

what are the most common symptoms of anaphylaxis in intraop patient

A

hypotension
tachy
bronchospasm
THEN
hypovolemia
shock
hypoxemia

365
Q

what is the definitive treatment for anaphylaxis intraop

A

epi

366
Q

what do you do for anaphylactic patient intraop

A

epi
IV fluids
vasopressin

367
Q

what is an example of an H2 antagonists

A

ranitidine

368
Q

what are examples of b2 agonists

A

albuterol, terbutaline,

369
Q

what medication can we give or airway edema

A

corticosteroids

370
Q

what are s/s grade 1 anaphylaxis

A

Cutaneous signs: generalized erythema, urticaria, angioedema.

371
Q

what are s/s grade 2 anaphylaxis

A

Cutaneous signs, hypotension, tachycardia, cough, difficult ventilation.

372
Q

what are s/s grade 3 anaphylaxis

A

Hypotension, tachycardia or bradycardia, arrhythmias, bronchospasm.

373
Q

what are s/s grade 4 anaphylaxis

A

Cardiac and/or respiratory arrest, pulseless electrical activity (PEA).

374
Q

what mediates type 2 hypersensitivity reactions

A

IgM or IgG

375
Q

what are examples of type 2 reactions

A

type 1 DM
myasthenia gravis
drug-induced hemolytic anemia
granulocytopenia
thrombocytopenia
transfusion reactions
goodpastures nephritis

376
Q

what is treatment for type 2 reactions

A

anti-inflammatory
immunosuppressants

377
Q

what is another name for type 3 reaction

A

immune complex hypersensitivity

378
Q

what medaites type 3 reactions

A

IgG, IgM

379
Q

what differentiates type 2 and type 3 reactions

A

in type 3 antigen is soluble and not attached to tissue

380
Q

where are antibody-antigen complexes depositied in type 3 reactions

A

kidneys, skin, eyes

381
Q

how long does it take for type 2 reaction

A

minute to hours

382
Q

how long does it take for type 3 reaction

A

hours to weeks

383
Q

what are examples of type 3 reactions

A

serum sickness
systemic lupus erythematosus
RA

384
Q

what is another name for type 4 hypersensitivity

A

cell mediated or delayed type hypersensitivity

385
Q

what is onset of type 4 reaction

A

24 hours to 14 days

386
Q

what are the primary mediators of type 4 reactions

A

T lymphocytes
monocytes
macrophages

387
Q

what are examples of type 4 reactions

A

poison Ivy
TB
leprosy
PPD test

388
Q

what mediates type 5 hypersensitivity

A

autoantibodies that bind and stimulate specific target cells

389
Q

what is an example of type 5

A

graves (stimulates TSH receptor)

390
Q

why do we give FFP in angioedema

A

kininase 2 catalyzes the degredation of excessive bradykinin

391
Q

what are some anesthetic considerations for intubating angioedema

A

do not delay intubation
-use video/fiberoptic technique
-use precedex and ketamine for intubation to maintain resp drive
-give succs once you see cords

392
Q

what do you pretreat a protamine reaction wtih

A

pepcid
benadryl
calcium

393
Q

what are the first signs of protamine reaction

A

increased peak airway and severe vasodilation

394
Q

what is treatment for amniotic fluid embolism

A

A-OK
atropine
ondansetron
ketoralac

Adv Pharm II (3 decks)

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