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J - Pharm Final > Exam 4 Review > Flashcards

Exam 4 Review Flashcards

1
Q

Most common nerve and muscle monitored are:

A

Ulnar nerve

Adductor Pollicis muscle of the hand

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2
Q

Most common muscle monitored

A

Adductor Pollicis

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3
Q

What does dibucaine test for?

A

Test for atypical psuedocholinesterase

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4
Q

Accelomyography is used for what?

A

Monitoring

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5
Q

Acetylcholinesterase inhibitors work by

A

inhibiting AChE…. hydrolysis

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6
Q

What are side effects of cholenergic agents?

A

SLUDGE-M
Come from muscurinic AND cholinergic!

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7
Q

What is the ceiling effect?

A

After the max dose there is no more AChE at the junction to inhibit.
So neostigmine and edriphonium will not work with a deep block.
REVERSAL IN DEEP BLOCKADE LEADS TO FURTHER BLOCKADE

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8
Q

Reversal of NM blockade depends on what? (4)

A

Depth of NM block
AChE inhibitor of choice
Dose administered
Anesthesia agent of choice

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9
Q

Scenario: the patient has 0/4 twitches, what should we do?

A

Decrease the MAC since the patient has 0/4 twitches.
WAIT to give the reversal!

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10
Q

What is the DOA of edrophonium?

A

5-15 min

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11
Q

Scenario:
The patient is developing recurarization with vecuronium and was reversed with edrophonium. Why is this happening?

A

The DOA for edrophonium is not long enough! (only 5-15 min)

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12
Q

LTA (laryngotracheal anesthesia)

A

The black line should be at the vocal chords (the larynx)

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13
Q

Ooops! We gave a renal patient neostigmine! What will happen?

A

Neostigmine will be metabolised by the liver (30-50%) if there is no renal function.

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14
Q

Pulmonary side effects of Neostigmine and Edrophonium?

A

Brochoconstriction
AND
Increased airway resistance

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15
Q

Dose 4 mg neostigmine - if we want to give 100% glycopyrolate, how much do we give?

A

0.8 mg (4 mL)

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16
Q

Which anticholenergic is best for an MI patient?

A

Glycopyrrolate (slow over 2 min)

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17
Q

Persistant NM blockade… pesky guy… why isn’t my ACh working?

A

No further anticholenesterase is effective because there is only a finite amount of ACh available at the junction.

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18
Q

Which reversal is highly water soluble?

A

Sugammadex

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19
Q

What is the primary route of elimination for sugammadex?

A

urine

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20
Q

Where dose sugammadex work?

A

binds to free drug in the PLASMA

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21
Q

Which patients can recieve sugammadex?
Which patients cannot?

A

OK for deep block and cirrhosis patients

NOT ok for renal or bleed

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22
Q

What is the first treatment for recurarization?

A

Supplemental O2

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23
Q

What is added with epi to prevent oxidation of LA?

A

Sodium bisulfite

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24
Q

What is the DOA of chloroprocaine?

A

30-45 min
least/lowest/fastest DOA

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25
Q

Compare protein binding of Procaine, Lidocaine, and Bupivacaine (rank from least to most binding)

A

Procaine = 6
Lidocaine = 70
Bupivacaine = 95

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26
Q

Which is a rapid amide?

A

Lidocaine

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27
Q

What is the max dose of Lidocaine for spinal?

A

100 mg

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28
Q

What is the max bupivacaine (w/epi) dose?

A

175 –> 225

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29
Q

What is the max Lidocaine (w/ epi) dose?

A

300 –> 500

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30
Q

Most important components of:
Potency
DOA
Onset

A

Potency = lipid solubility
DOA = protein binding
Onset = pK

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31
Q

Where does LA bind?

A

INNER gate of sodium channel

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32
Q

How does LA MOA work?

A

No sodium comes in so the cell doesn’t reach threshold and can’t fire action potentials

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33
Q

What is blocked first?

A

Preganglionic B fibers –> fastest because they are SNS fibers

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34
Q

Highest blood concentration for uptake of LA

A

IV > TRACHEAL > caudal > paracervical > epidural > brachial > sciatic > SQ

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35
Q

Rate of clearance is affected by what? (2)

A

Cardiac output
Protein binding

36
Q

Adding epi changes LA by increasing duration by what?

A

1/3

37
Q

Esters metabolised by:

A

Cholinesterases in the PLASMA

38
Q

Esters metabolite:

A

ParaAminoBenzoic Acid (PABA)

39
Q

Amides metabolised by:

A

Liver metabolism (slower than esters)

40
Q

Bupivacaine and Ropivacaine protein binding site

A

Alpha-1 acid glycoprotein

41
Q

Procaine

A

excreted unchanged in the liver?

42
Q

What is the most likely component that a patient is allergic to?

A

Usually the preservative

43
Q

DOC for inhalation for respiratory or intubation?

A

Lidocaine

44
Q

Which drug has increased protein binding resulting in decreased maternal:fetal ratio and is the least likely to ion trap?

A

Bupivacaine

45
Q

Metabolism order of LAs from slowest to fastest:

A

Bupivacaine (95%)
Lidocaine (70%)
Prilocaine (55%)

46
Q

Metabolite of prilocaine that causes methemoglobinemia?

A

Orthotoluidine

47
Q

Methelyne blue dose for an 80 kg patient?

A

80 mg

1-2 mg over 5 min
remember max 8mg/kg

48
Q

Which LA for most cardiac toxcicity?

A

Bupivacaine

49
Q

Which LA has either slowest metabolism or highest protein binding?

A

Levobupivacaine (>97% protein bound)

50
Q

Most likely LA for LAST?

A

Bupivacaine > ropivacaine > lidocaine > chloroprocaine

51
Q

Which LA is an ester but is metabolised by the liver?

A

Cocaine

52
Q

What does alkinazation of LA do? (2)

A

Increases % of lipid soluble form
Shortens onset

53
Q

What do adjuncts do with LA?

A

Increase DOA

54
Q

How to negate fast spread of LA?

A

Vasoconstrictor (basically add epi)

55
Q

LA is administered where?

A

Around the nerve

56
Q

Which LA causes methemoglobinemia?

A

Benzocaine
AND
Prilocaine

57
Q

DOA of LA is proportional to what?

A

time in contact with nerve fibers

58
Q

Signs of systemic absorption?

A

HR change and HTN

59
Q

Based on the graph that we cannot see here, adding epi does what?

A

LA stays local longer so there is decreased systemic absorption.

60
Q

Know epi math!

A

1:200,000
0.25% is 2.5 mg/mL

61
Q

Which LA has fastest liver metabolism? why?

A

Prilocaine > Lidocaine > Bupivacaine

Due to protein binding

62
Q

EMLA is composed of what?

A

Lidocaine and Prilocaine

63
Q

SQ injection of LA

A

Doubled by adding epi 1:200,000

64
Q

Which tissues are blocked first with a peripheral nerve block?

A

PROXIMAL first
then distal

65
Q

Onset of PNB depends on what?

A

depends on LA pKa

66
Q

LA duration depends on what?

A

DOSE

67
Q

What do you need for IV regional or beir block?

A

tourniquet
IV

68
Q

Confirmation of SAB?

A

CSF

69
Q

Site of action for SAB?

A

Preganglionic fibers is the principle site of action

70
Q

How to assess block? (3)

A

Sensory is at the level of denervation
SNS is 2 segments up (cephalad)
Motor is 2 segments down (caudal)

71
Q

T4 is at what anatomical point?

A

The nipple line!

72
Q

If a patient is getting SAB and 5’2”, how much do we give?

A

1.2 mL (1 mL then 0.1 mL for every inch > 5 ft)

73
Q

What is more important for SAB?

A

DOSE

74
Q

Specific gravity of LA determines the spread… (hyperbaric vs. hypobaric)

A

Hyperbaric sinks d/t dextrose
Hypobaric floats

75
Q

Scenario:
Patient is getting a left hip and we are using hyperbaric, how do we lay them?

A

Right lateral

76
Q

Most common neuro effect of lidocaine?

A

Circumoral numbness

77
Q

Tumescent liposuction epi 1:100,000 what is the concentration of epi?

A

10mcg/mL

78
Q

Tumescent liposuction what is diluted lidocaine conc?

A

0.05% to 0.10%

79
Q

Tumescent liposuction with diluted lidocaine and 1:100,000 epi - dose calculation for 100kg person?

A

3500 mg
OR
5500 mg

80
Q

Treatment of systemic toxicity?

A

Prompt airway managment –> supplemental O2

81
Q

LAST lipid emulsion therapy math

A

Bolus 1.5 mL/kg of 20% lipid emulsion

20% = 200 mg/mL

82
Q

Infusion with LAST dose over how long?

A

0.25 mL/kg/min
Over 10 min

83
Q

Transient neurological treatment; select 2

A

trigger point injections
NSAIDS

84
Q

How long does methelyne blue reduce?

A

60 min

85
Q

Cocaine chest pain or vasospasm treatment:

A

Benzos (versed)
Nitroglycerin

86
Q

DOC for nasal/ENT case

A

Cocaine

J - Pharm Final (20 decks)

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