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Pharm > Anesthetics II > Flashcards

Anesthetics II Flashcards

1
Q

What are the major disadvantages of local anesthesia?

A

Potential for systemic toxicity if use large enough amounts

Poor minute-minute control

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2
Q

Procaine = ?

A

Novocain

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3
Q

What is perineural infiltration of anesthetics?

A

Nonspecific injection of the agent at one or more sites around specific area

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4
Q

What is regional nerve blocks?

A

Inject around a specific nerve to block sensory and motor fibers distal to the block

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5
Q

What is the major advantage and major disadvantage to nerve blocks?

A

Advantage = less drug required

Disadvantage = Require more skill and anatomical knowledge

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6
Q

What is the MOA of a spinal block?

A

Injection of an agent into the lumbar subarachnoid space to read the roots of the spinal nerves that supply a specific region

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7
Q

True or false: once in the spinal canal, there are no barriers to keep a drug from reaching the brain

A

true

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8
Q

What are the two main advantages of spinal blocks?

A

More reliable; return of CSF indicates correct placement

Pt is conscious with minimal disruption of heart/lungs

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9
Q

What are the major disadvantages of spinal blocks?

A

Not reversible

No titration

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10
Q

Why can spinal blocks lead to hypotension?

A

Blockage of sympathetic innervation to the distal regions of the block

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11
Q

What is an epidural block?

A

Inject into the extradural space and block the root as it passes through the space

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12
Q

What is the major advantage to epidurals?

A

Not time limited

Can be titrated

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13
Q

What is the major disadvantage to an epidural?

A

Less reliable than spinal block

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14
Q

What is the way to inject IV anesthesia locally?

A

Inject with tourniquet, but will eventually go through circulation, so not used often

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15
Q

For the ideal local anesthetic, do you want it to be short or long lasting?

A

Short

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16
Q

What is the MOA of brain signalling of pain? What signalling pathway is utilized? Where does this cross?

A

Local release of bradykinin, substance P causes activation of local spinothalamic fibers, which crosses at and above the level, and ascends to the sensory cortex

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17
Q

What is the MOA of local anesthetics?

A

Block the transient increase in Na channel permeability, thereby raising the threshold for excitability

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18
Q

Is the resting permeability of K affected by local anesthetics?

A

Yes

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19
Q

What happens to local anesthetics when they enter the body? How do they get into a cell?

A

Deprotonated, which allows them to cross the lipid bilayer

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20
Q

Which side of the Na channels do local anesthetics work on: intracellular or extracellular side?

A

Intracellular

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21
Q

What are the local anesthetics that bind to the outside of the Na channel?

A

Biotoxins

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22
Q

What is the MOA of lidocaine?

A

Binds to the intracellular side of the Na channel, preventing its opening

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23
Q

What is the MOA of benzocaine?

A

Gets into the lipid bilayer, and changes the conformation of the Na channel (membrane expansion theory)

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24
Q

What is the MOA of most locally used anesthetics?

A

Binds to the intracellular Na channel binding site

Interrupts the geometry of lipid bilayer

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25
Q

What is the MOA of tetrodotoxin? Where does this come from?

A

Pufferfish toxin that binds to the outside of the local Na channels, and prevents opening of the channel

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26
Q

What are the two chemical structural parts of all local anesthetics? Why is each important?

A

Aromatic ring for lipophilicity to pass through membrane

Tertiary amine (polar) for binding

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27
Q

What are the two general classification of local anesthetics (based on chemical structure)? What differentiates each agent within each of these groups?

A

Amides
Esters

The intermediate chain (between the amide/ester and the tertiary amine group)

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28
Q

What is the suffix associated with local anesthetics?

A

“-caine”

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29
Q

What is the rule for differentiating amides from esters?

A

Generally, amides have two “i”s in their name, while esters have one

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30
Q

Amide or ester: lidocaine

A

Amide

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31
Q

Amide or ester: cocain

A

Ester

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32
Q

Amide or ester: articaine

A

Amide

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33
Q

Amide or ester: mepivacaine

A

Amide

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34
Q

Amide or ester: procaine

A

Ester

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35
Q

Amide or ester: etidocaine

A

Amide

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36
Q

Amide or ester: benzocaine

A

Ester

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37
Q

Amide or ester: tetracaine

A

Ester

38
Q

Amide or ester: Prilocaine

A

Amide

39
Q

Amide or ester: Bupivacaine

A

Amide

40
Q

Amide or ester: chloroprocaine

A

Ester

41
Q

Amide or ester: ropivacaine

A

Amide

42
Q

Amide or ester: levobupivacaine

A

Amide

43
Q

What type of chemical are all local anesthetics: weak bases, weak acids, strong bases, or strong acids?

A

Weak bases

44
Q

What is the uncharged form of local anesthetics important for?

A

Lipid penetration of membranes

45
Q

What is the charged forms of local anesthetics useful for?

A

Active form at Na receptor

46
Q

How are amides metabolized? Esters? Which, therefore, is impaired with hepatic problems

A 
Amides = p450s **hepatic
Esters = butyryl cholinesterases
47
Q

What is the relative half life of amides? Esters?

A 
Amides = Long
Esters = short (
48
Q

What is the minimum anesthetic concentration (Cm)?

A

Minimum concentration of drug for standard block (relative standard of potency)

49
Q

How does the size of the neuronal fiber that is being blocked relate to the Cm needed to block it?

A

increased fiber size = increase Cm needed

50
Q

What is order of fibers that are blocked, from first to last? (hint: same order as smallest to largest)

A 
B fibers
C fibers
A-delta
A-gamma
A-beta
A-alpha
51
Q

Are C fibers myelinated? What information do they carry?

A

No

Slow pain and temp

52
Q

What are A-alpha fibers used for?

A

motor/proprioception

53
Q

What are A-beta fibers used for?

A

Discriminative touch

54
Q

What are A-delta fibers used for?

A

Fast pain, temp, crude touch

55
Q

What are B fibers used for?

A

Preganglionic fibers

56
Q

What is the standard of potency for local anesthetics?

A

Cm

57
Q

Which are affected first: myelinated or unmyelinated fibers?

A

Myelinated

58
Q

What is the relationship between pH and local anesthetic Cm?

A

Increased pH means lower Cm needed

59
Q

What is the relationship between [Ca] and Cm?

A

Increased [Ca] = Increased Cm

60
Q

What is the relationship between nerve stimulation rate and Cm?

A

Higher frequency nerves are most sensitive to LA

61
Q

Why are vasoconstrictors added to LA preparations?

A

Stays local longer

Increases duration of action

62
Q

What is the vasoconstrictor commonly used with LAs?

A

Epi

63
Q

What are the areas that should never be injected with LA that have epi? (5) Why?

A 
Digits
Toes
ear Lobes
Nose
Penis

All have arterioles, and have the potential to develop sloughing off of tissue

64
Q

What are the four factors that affect reversal of LAs?

A
  1. Dilution by ECF
  2. Absorption into circulation
  3. Redistribution to other areas
  4. use of vasoconstrictors
65
Q

What is the most important factor that affects the reversal of LAs?

A

Absorption into circulation

66
Q

What are the two factors that are involved in redistribution of LAs?

A

Organ blood flow and plasma protein binding

67
Q

Where are amides/esters metabolized

A 
Amide = liver
Esters = plasma by BChE
68
Q

What is the metabolite that is produced by metabolism of esters? Why is this concerning?

A

Para-Aminobenzoic acid (PABA)

May cause allergic reaction

69
Q

True or false: there is cross reactivity between esters and amides. Thus if a pt is allergic to one group, they are likely allergic to the other

A

False

70
Q

Why are esters less likely to have systemic toxic effects?

A

Rapid metabolism in the blood

71
Q

Most of the allergic reaction in LA are actually due to what preservative?

A

Methylparaben

72
Q

Systemic toxicity of what LA can cause Cardiac collapse and death d/t its selectivity

A

Bupivacaine

73
Q

What is the treatment for local anesthetic systemic toxicity (LAST)? MOA?

A

IV lipid emulsion (intralipid)

Forms a sink for the LA

74
Q

What is the reference standard for amide LAs?

A

Lidocaine

75
Q

What is the LAs that can be used both topically and via injection?

A

Lidocaine

76
Q

If attempting to give an epidural for a c-section, what LA would you use?

A

Lidocaine

77
Q

What is the toxic effect of lidocaine?

A

Transient neurologic symptoms (with spinal administration

78
Q

What is the clinical use of bupivacaine?

A

Agent of choice for epidural infusion for labor analgesia and post-op pain

79
Q

True or false: bupivacaine is an excellent spinal anesthetic?

A

True

80
Q

What are the toxic effects of bupivacaine?

A

CNS excitation and cardiac collapse

81
Q

What is the less toxic form of bupivacaine?

A

Levobupivacaine

82
Q

What is the clinical use of articaine?

A

Dental anesthetic

83
Q

What is the clinical use of cocaine?

A

Topical anesthetic for HENT procedures

84
Q

What is the clinical uses for benzocaine?

A

Topical only anesthetic,

85
Q

What is the clinical use of chloroprocaine

A

epidural agent for labor

86
Q

What is exparel-liposome?

A

Encased bupivacaine in a liposome, that is given post op for pain

87
Q

What is EMLA? Clinical use?

A

Eutectic mixture of Local Anesthetics (lidocaine + prilocaine)

Topical anesthetic

88
Q

What is TAC? Clinical use?

A

Tetracaine
Adrenalin
Cocaine

Topical used in pediatric emergencies

89
Q

What are neurolytics?

A

Agents that are not reversible, and achieve a permanent local anesthesia

90
Q

What are the two prototypical neurolytics?

A

Ethyl alcohol

Phenol

Pharm (73 decks)

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